Anesthetic Considerations Anesthetic Considerations of Physiological Changes of Physiological Changes

During PregnancyDuring Pregnancy

Presented by:Mona Abdelsamie

Assistant lecturer of AnesthesiologyUnder Supervision of:Prof. Dr. Hoda Omar

Professor of Anesthesiology & Intensive careAnesthesiology Department

Ain Shams University

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OBJECTIVESOBJECTIVES

Maternal physiology during Maternal physiology during pregnancy.pregnancy.

Uteroplacental circulation.Uteroplacental circulation. Placental transfer of anesthetic Placental transfer of anesthetic

agents.agents. Effect of labor on maternal Effect of labor on maternal

physiology.physiology.

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Anaesthesia for parturient

What is the difference?

Anaesthesia for parturient

What is the difference?

Physiologicalchanges

Alter the usual response

to anaesthesia

2 Patients are caredFor simultaneously

Mother Fetus

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Maternal Physiology during PregnancyMaternal Physiology during Pregnancy

1) Progressive MAC.1) Progressive MAC.

by 40% at termby 40% at term

Returns to normal by 3Returns to normal by 3rdrd day day

postpartum. postpartum.

CNS

Progesterone increases20 times normal

level at term

β- endorphin surge during labor & delivery

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2 ↑ )Sensitivity to Local Anesthetics.

LA requirements during RA ↓ by 30% .

Hormonally Mediated

Engorged Epidural Venous Plexus

↓CSF Volume

↓Volume ofEpidural Space

↑Epidural space Pressure

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"ٌRespiratorysystem

↑Oxygen consumption20 – 40%

↑Minute Ventilation40 – 50%

↑↑VT & ↑ RR

&↑P50 (30 mmHg) ↑PaO2 ↓PaCo2 (28-32 mmHg)

Compensatory ↓ HCo3ˉ

Progesterone ↑CO2 Production

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IRVIRV

2000m2000mll

++5%5%

IC2650m

l+15%

VCVC3500m3500m

llNo No

ChangeChange

TLCTLC4550m4550m

ll

--5%5%

VTVT650ml650ml

++45%45%

ERVERV850ml850ml

--25%25%FRCFRC

1900m1900mll

--20%20%RVRV1050m1050m

ll

--15%15%

Volumes Capacities

Lung volumes & capacities at term gestation in absolute volumes & as the percentage change from non-pregnant Values.

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↓FRC + ↑O2 Consumption

=Rapid desaturation during

periods of apnea.

☼Pre-oxygenation prior to GA is mandatory.☼Parturient Should not lie flat without

supplemental oxygen.

↓FRC & ↑MV↑ ☼Uptake of Inhalational

Anesthetics.

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Hormonal Changes Capillary engorgement of respiratory tract mucosa

1 ) ↑Incidence of difficult intubation.2 (Trauma and bleeding during

endotracheal intubation.

☼Use a small ETT (6 – 7 mm) during GA

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HematologicalChanges

I : ↑ Blood Volume ( up to 90ml/ Kg)

↑by 1000 – 1500 ml at term.Returns to normal 1 – 2 weeks postpartum.

↑Plasma Volume > ↑ RBC mass

+

=

Dilutional anemia & ↓ blood viscosity

Facilitates maternal & fetal exchange of respiratory gases,

nutrients & metabolites

↓Impact of maternal blood loss at delivery

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II : Hypercoagulable state

↑Fibrinogen, factors VII, VIII, IX, X & XII

↓Factor XI

III : Other changes:

* Leucocytosis up to 21,ooo/µL.* 10-20% ↓ in platelet count.* Marked ↓ cell mediated immunity→ ↑susceptibility to viral infection.

Risk Of DVTOne of the leading causes of maternal mortality

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CVS ↑COP by 40% at term

↑HR 15 – 30% ↑ SV 30%

Returns to normal 2 weeks postpartum.

↓SVR → ↓ SBP & ↓↓ DBP, the response to adrenergic and vasoconstrictor agents is decreased.

CVP, PAP, PAWP → unchanged.

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Supine Hypotension syndrome

COP ↓ in supine position after 28th week of gestation.

Occurs in 20% of women at term.

Compression of IVC Compression of lower aorta

Aortocaval compression

↓blood flow to kidneys, uteroplacental

circulation& lower extremeties

↓VR → ↓ COP by 24% at term.

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Compensatory mechanisms in unanaesthetised Women

Venous Collaterals

ParavertebralVenous plexus

Abdominalwall

↑SVR & HR

Reduced during general or regional anesthesia.

Severe Hypotension

Profound Fetal Hypoxia

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No woman in late pregnancy should lie supine without shifting the uterus off the great abdomino-pelvic vessels.

Left lateral decubitus

Tilting the tableLeft side down

Rigid wedge under The right hip

Fluid preloading before neuroaxial anesthesiaIt does not completely avoid maternal hypotension but

it↑ maternal COP → preserve uteroplacentalblood flow.

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GIT

☼Upward displacement of the stomach by the uterus → Incompetence of gastroesophageal sphincter → Gastroesophageal reflux & esophagitis.

The parturient should be considered a full stomach patient during most of gestation

↑ ☼Progesterone → ↓ tone of gastroesophageal sphincter.

☼Placental Gastrin → Hypersecretion of gastric acid.

☼Gastric emptying → Delayed with labor.

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Pharmacological prophylaxis against aspiration.

No positive pressure ventilation before intubationRapid sequence induction.

Sellick’s maneouvre

For GA:

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RenalSystem

♦RBF & GFR ↑ by 50% at 1st trimester but returns to normal in 3rd trimester.

↑♦ Renin & Aldosterone → Na+ retention.

♦Sr. Creatinine & BUN may ↓ to 0.5 – 0.6mg/dL& 8 – 9 mg/dL respectively.

↓♦Renal tubular threshold for glucose & amino acids → mild glycosuria (1-10g/d) & proteinuria (< 300mg/d).

♦Plasma osmolality ↓ by 8 – 10 mosm/Kg.

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HepaticEffects

♦Hepatic function & hepatic blood flow→ unchanged.

♦Minor ↑ in Sr. Transaminases & LDH in 3rd trimester.

↑♦Sr. Alkaline phosphatase (placental).

♦Mild ↓ in Sr. albumin (dilutional).

♦25 – 30% ↓ in pseudocholine estrase activity.

↑♦Progesterone levels→ inhibit release of cholecystokinin→ incomplete emptying of gall bladder→ altered bile acid composition→ formation

of cholesterol stones.

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MetabolicEffects

Pregnancy is Diabetogenic

Human Placental lactogen→ relative insulin resistance.

Starvation like state

↓Blood Glucose & Amino Acid levels. ↑Free Fatty Acids, Ketones & triglycerides .

↑Estrogen levels→Thyroid gland hypertrohy→ ↑ T3 & T4

↑TBG → Free T3, T4 & TSH remain normal

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Uteroplacental Circulation

At term: uterine blood flow is 10% of COP

≈600 – 700 ml/min.

80% to placenta

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Maximally dilated uterine vasculature with absent autoregulation.

Uterine Blood Flow

Directly proportional to difference betweenuterine arterial and venous pressure.

Inversely proportional to uterine vascular resistance.

Abundant α-adrenergic & some β-adrenergic receptors .

Previously , vasoconstrictor agents with predominant β-adrenergic activity (e.g. Ephedrine )were of choice for hypotension during pregnancy.

Recent studies show that α-adrenengic drugs (e.g.Phenylephrine) have better effects.

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3 major factors ↓ uterine blood flow during pregnancy

SystemicHypotension

UterineVasoconstriction

Uterine Contractions

♦Aortocaval compression.

♦Hypovolemia.

♦Sympathetic blockwith regional anesthesia.

♦stress-induced endogenousCatecholamines during labor.

♦α-adrenergic agonists.

♦Local anesthetic agents.

♦Hypertensive disorders →generalized vasoconstriction.

♦Labor.

♦Oxytocin infusions.

♦Extreme hypocapniaPaCO2 < 20 mmhg.

♦Barbiturates& Propofol.

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Placental transfer of anesthetic agents

Placental transfer of drugs depends on:

1 :Molecular weight : < 500 Da cross easily.

2 :Protein binding.

3 :Lipid solubility: Highly ionized substances have poor lipid solubility.

4 :Maternal & fetal pH : affect ionization of the drug.

5 :Maternal drug concentration: affected by dose given and route of administration.

6 :Timing of administration.

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Inhalational Agents

Cross placenta freely

Limited effects if < 1MAC & delivery within 10 min. of induction Intravenous

Agents :

Thipental, ketamine & propofolLimited fetal effects

in usual induction doses

(drug distribution, metabolism & placental uptake)

OpioidsCross placenta freely

Variable effects.

MorhineMost significant respiratory depressant

effects MeperidineMeperidineSignificant respiratory depression peaking

1- 3 h after administration.

FentanylMinimal effect if < 1µg/Kg.

Muscle RelaxantsThe highly ionized property impedes placental transfer.

Minimal effects on fetus.

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Local anesthetics → Placental transfer depends on:

1 :pKa.

2 :Maternal & fetal pH : Fetal acidosis → higher fetal to

maternal

drug ratios . Binding of hydrogen ions to the nonionized form

→ trapping

of local anesthetic in fetal circulation

3 :Degree of protein binding : highly protein bound agents

diffuse poorly across the placenta.

Chloroprocaine has the least placental transfer as it is rapidlybroken down by plasma cholinestrase in the maternal circulation.

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Most of anesthetic agents show significant placental transfer

Fetal effects of drugs administered to parturient depend on:

1: Maturity of fetal organs, substantial fetal hepatic uptake of many drugs.

2 :Dilution of the umbilical venous blood by venous blood from lower half of fetal body → modify fetal

drug distribution.

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Effect of labor on maternal physiology

Stages of labor

1st stage 2nd stage 3rd stage

Starts with true labor pains, ends by full cervical dilation.

Starts with full cervical dilation, fetal descent

occurs, ends with complete delivery of fetus.

Extends from birth of the baby to delivery of theplacenta.

Latent phase Active phase

Progressive cervical effacement &minor dilataton (2 – 4 cm) .

Progressive cervical dilatationup to 10 cm.

8 – 12 h in nulliparous5 – 8 h in multiparous.

Contractions are 1.5- 2 min apart, last 1 – 1.5 min

15 – 120 min.

15 – 30 min.

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Intense painful contractions

Maternal hyperventilationMV ↑ up to 300%.

↑O2 consumption 60% above 3rd trimester values

PCo2 < 20 mmHg

Uterine VC → Fetal acidosis+

Periods of hypoventilation → transient maternal & fetal hypoxemia in betweenContractions.

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Each contraction

Displaces 300 – 500ml blood from uterus to central circulation.

COP ↑ 45% above 3rd trimesteric value.

Maximum strain on the heart occurs immediately after delivery.

Uterine intense involution→ sudden relieve of IVC ↑ →COP 80% above prelabor values.

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DiscussionDiscussion

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Questions

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Fetal blood concentrations of lidocaine Fetal blood concentrations of lidocaine following maternal administration would be following maternal administration would be higher than expected:higher than expected:

1.1. If administered during uterine contraction.If administered during uterine contraction.

2.2. In the presence of umbilical cord In the presence of umbilical cord

compression.compression.

3.3. In the presence of maternal acidosis.In the presence of maternal acidosis.

4.4. In the presence of fetal acidosis.In the presence of fetal acidosis.

5.5. In the presence of increased maternal In the presence of increased maternal

metabolism.metabolism.

X

X

X√

X

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1. Total peripheral resistance decreases.2. Hb concentration decreases.3. Plasma cholinestrase concentration

increases.4. Blood glucose concentration increases.5. Functional residual capacity increases.

During pregnancyDuring pregnancy::

√

√X

X

X

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The dose of bupivacaine required for spinal The dose of bupivacaine required for spinal anesthesia is reduced in the pregnant patient anesthesia is reduced in the pregnant patient at term because of decreasedat term because of decreased: :

1. CSF volume.2. Spinal cord blood flow.3. Metabolism of bupivacaine.4. CSF pressure.5. Turnover of CSF.

√X

XX

X

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1. Maternal arterial pH.2. Fetal cerebral blood flow.3. Maternal cerebral blood flow.4. Maternal uterine artery flow.5. Fetal arterial PO2.

Maternal hyperventilation produces a decrease inMaternal hyperventilation produces a decrease in::

X

X

√

X

√

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The following substances transfer freely The following substances transfer freely across the placenta:across the placenta:

1.1. Neostigmine.Neostigmine.

2.2. Insulin.Insulin.

3.3. Pancuronium.Pancuronium.

4.4. Atropine.Atropine.

5.5. glycopyrolate.glycopyrolate.X

√X

X√

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Thank you