Presenter:- Dr. SHALINIModerator:- Dr. PUNEET

Pregnancy produces profound physiological changes(adaptive to stress) that become more significant as pregnancy progresses in duration.

This changes can be due to:-

1) Hormonal alteration,

2) Mechanical effect of gravid uterus,

3) Increased oxygen & metabolic requirement,

4) Haemodynamical alteration.

In addition unique challenges - two patients are cared for simultaneously, failure to take care can be disastrous for one or both of them.

Parameter Change

Blood volume + 30%

Plasma volume + 45%

Cardiac output + 30-50%

Stroke volume + 20-50%

Heart rate + 15-25%

Peripheral resistance - 15-20%

CVP, PCWP Unchanged

Fluid retention is the most fundamental systemic change of normal pregnancy.

The total plasma volume is increased during pregnancy 45%. The most marked expansion occurs in extra cellular volume (ECV) with some increase in intra cellular water.

The factors contributing –

Increase sodium retention.(RAAS)

Decrease in thirst threshold.

Decrease in plasma oncotic pressure(↓ plasma albumin levels)

At term, maternal blood volume has increased by 1000—1500 mL in most women, allowing them to easily tolerate the blood loss associated with delivery.

Normal delivery = 400-500ml blood loss

Cesarean section = 800-1000ml blood loss

Blood volume does not return to normal until 1—2 weeks after delivery

Cardiac output(40%) increases to meet accelerated maternal and fetal metabolic demands. This increase is mostly due to an increase in stroke volume (30%) as heart rate increases only slightly (about 15%).

Heart rate elevation occurs in response to increased oxygen demand.

CO ↑ 40% by 12 weeks

50% for rest of pregnancy

60%-100% during labor & after delivery

CO highest right after delivery (release of aorto-caval compression) due to uterine contraction.

Peripheral vascular resistance (VR) decreases due to the vasodilatory effects of progesterone and the proliferation of low resistance vascular beds in the inter-villous spaces of the placenta.

Because of the decrease in peripheral vascular resistance(in spite of increased CO), arterial bloodpressure does not significantly change or may show a slight fall in an uncomplicated pregnancy.

Diastolic(20%) > Systolic(8%) The response to adrenergic agents and vasoconstrictors is

thus blunted.

Despite the increase in blood volume, there is no change in the central venous pressure(CVP) during pregnancy. This is most likely due to dilated systemic and pulmonary circulations.

Cardiac chambers enlarge and myocardial hypertrophy is often noted on echocardiography.(Eccentric due to activation of RAAS).

Also show variable ECG,

ECHO, CXR Changes.

9

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 cervicaldilation, fetal descentoccurs, ends with complete delivery of fetus.

Extends from birth of the baby to delivery of theplacenta.

Latent phaseActive phase

Progressive cervical effacement& minor dilatation (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.

10

Intense painful contractions

Maternal hyperventilationMV ↑ up to 300%.

↑ O2 consumption 60% above 3rd trimester values

Marked Hypocapnia PaCo2 < 20 mmHg

Uterine Vasoconstriction (fetal acidosis)

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

11

Each contraction

Displaces 300 – 500ml blood fromuterus to central circulation.

CO ↑ 45% above 3rd trimesteric value.

Maximum strain on the heart occurs immediately after delivery.

Uterine intense involution→ sudden relieve of IVC→ ↑ COP 80% above pre-labor values.

Effect of Pregnancy on Cardiovascular Investigations

Investigation Findings

Chest radiography Apparent cardiomegaly

Enlarged left atrium (lateral views)

Increased vascular markings

Straightening of left-sided heart border

Postpartum pleural effusion

ECG Right-axis deviation

Right bundle branch block

ST-segment depression on left precordial leads

Q waves in lead III

T-wave inversion in leads III, V2, and V3

Rotation of 15 degrees(QRS axis)

ECHO Trivial tricuspid regurgitation

Pulmonary regurgitation (up to 94% at term)

Increased left atrial size by 12%-14%

Increased left ventricle end-diastolic dimensions by 6%-10%

Inconsistent increase in left ventricle thickness

Mitral regurgitation (28% at term)

Pleural effusion (40% postpartum)

Occurs in 20% of women at term.

Aorto-caval compression

Compression of IVCCompression of lower aorta

↓ COP by 24% at term.↓ blood flow to kidneys,utero-placental circulation &lower extremities

Supine Hypotension syndrome(hypotension associated with pallor, sweating, or nausea and vomiting)

Decreases in cardiac output can occur in the supine position after the 28th week of pregnancy.

Fetal hypoxia

Compensatory mechanisms in

unanaesthetised Women

Venous Collaterals↑ SV , ↑ HR & ↓ SVR

Para vertebralVenous plexus

Abdominalwall

Reduced during general or regional anesthesia.

Severe Hypotension

Profound Fetal Hypoxia

Women with a 28-week or longer gestation should not be placed supine without left uterine displacement.

Can be done by

Left lateral decubitus

Tilting the tableLeft side down

Rigid wedge (>15 degree) under

The right hip

Fluid preloading before neuro-axial anesthesiaIt does not completely avoid maternal hypotension but

It ↑ maternal CO → preserve utero-placental

blood flow.

Physical examination of the term pregnant woman may also be abnormal with auscultation commonly revealing a wide, loud, split first heart sound, an S3 sound, and a soft systolic ejection murmur.

Hence it is essential to differentiate the abnormal cardiovascular changes from normal physiological changes of pregnancy.

• Criteria to diagnose cardiac disease during pregnancy:

1) Presence of diastolic murmurs.

2) Systolic murmurs of severe intensity (grade 3).

3) Unequivocal enlargement of heart (X-ray).

4) Presence of severe arrhythmias, atrial fibrillation or

flutter

Changes in the respiratory system during pregnancy involve the upper airways, minute ventilation, lung volumes, and oxygen consumption.

Major physiological changes occur in the respiratory system during pregnancy due to a combination of both hormonal and mechanical factors.

Dyspnoea is a common complaint in pregnancy affecting over half of women at some stage.

Respiratory Parameter Change

Oxygen consumption + 20 to 50%

Minute ventilation + 50%

Tidal volume + 40 %

Respiratory rate Unchanged/ Slight increase(+10-15%)

PaO2 + 10%

PaCO2 - 15%

HCO3 - 15%

FRC (functional residual capacity) - 20%

From Birnbach DJ, Gatt SP, Datta S (eds): Textbook of Obstetric Anaesthesia. New York, Churchill Livingstone, 2000, p 35.

Due to increased metabolic demands, Oxygen consumption (+ 20 - 50%) and minute ventilation (+40 - 50%) progressively increase during pregnancy. (Increased progesterone sensitizes the central respiratory center to carbon dioxide – directly stimulating ventilation)

The pregnant woman thus takes larger Tidal volumes(40-50%) to eliminate carbon dioxide.

PaCO2 decreases to(28—32 mm Hg); significant respiratory alkalosis is prevented by a compensatory

↓ in plasma HCO3 concentration.

Hyperventilation may also increase PaO2.

Elevated levels of 2,3-diphosphoglycerate offset the effect of hyperventilation (↓PaCO2) on hemoglobin affinity for oxygen.

The combination of increased 2,3-DPG with increase in cardiac output enhances oxygen delivery to tissues.

The maternal respiratory pattern changes as the uterus enlarges

Diaphragm rises up(4cm) compensatory increases in

Antero-posterior diameters

Diaphragm motion not restricted

Chest wall motion limitation

Thoracic breathing favored over Abdominal

20% decrease in FUNCTIONAL RESIDUAL CAPACITY(FRC).

* No change in CLOSING CAPACICITY (CC) & VITAL CAPACITY

↓ FRC + ↑O2 Consumption + Unchanged CC

Rapid O2 de-saturation during periods of apnea (diminished capacity to

tolerate apnea).

Supine Position & Regional Block further diminishes FRC

Pre-oxygenation prior to induction of generalanesthesia should be given to avoid hypoxemia inpregnant patients.

Rapid development of hypoxemia

Rapid gaseous induction

The decrease in FRC coupled with the increase in minute ventilation accelerates the uptake of all inhalational anesthetics.

↓FRC → less dilution

↑MV → rapid deep depth

26

Hormonal Changes Capillary engorgement of respiratory tract mucosa

1) ↑ Incidence of difficult intubation.

2) Trauma and bleeding during endotracheal intubation.

☼ Repeated attempts at laryngoscopy must be minimized

☼ Use a small ETT (6 – 7 mm) during GA

1) Progressive decrease in MAC .

40% at term

(Returns to normal by 3rd day postpartum).

Progesterone increases20 times normal

level at term

β- endorphin surge duringlabor & delivery

LA requirements for subarachnoid or epidural anaesthesia are reduced in pregnancy (30%)

a) ↑ diffusion of LA to the receptor site.

b) ↑ sensitivity of nerve fibers to LA (Lower concentration needed).

c) engorged epidural venous plexus.

Spinal ligaments including ligament flavum SOFT hence loss of resistance technique used for regional block may be masked

CNS : its anaesthetic importance

IVC obstruction by enlarging

uterus

Engorged Epidural Venous Plexus

1) ↓CSF Volume

2) ↓Volume ofEpidural Space

3) ↑Epidural space Pressure

1,2: This enhances the cephalad spread of LA during regional blocks.

3 : Predisposes to higher incidence of Dural puncture & intravascular injection

The parturient should be considered a full stomach patient

during most of gestation

☼ Upward & ant. displacement of the stomach by the uterus → Incompetence of gastro-esophageal sphincter → Gastro-esophageal reflux & aspiration.

☼ ↑ Progesterone → ↓ tone of gastro-esophageal sphincter.

☼ Placental Gastrin → Hyper-secretion of gastric acid.

☼ Gastric emptying → Delayed with labor.

Narcotics and anti-cholinergic reduce lower

oesophageal sphincter pressure (used with precaution)

For GA:Pharmacological prophylaxis against aspiration.

Supine position with lateral tilt

No positive pressure ventilation before intubation

Rapid sequence induction.

Sellick’s maneuver

Renal vasodilatation increases renal blood flow early during pregnancy.

↑ Cardiac output(CO) ↑ GFR & ↑ RPF(renal plasma flow) by 50%.

↑ Renin & Aldosterone level promotes Na+ retention leading to volume overload.

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

↑ GFR ↑ clearance of urea, uric acid and creatinine

↓ plasma concentrations of

sr. Creatinine & BUN

BUN and Creatinine levels that would be considered marginally elevated in pre-pregnant patients are usually indicative of severe renal impairment in pregnancy.

Hepatic function and blood flow are unchanged.

A mild ↓ in serum albumin is due to an expanded plasma volume. Thus, the free fraction of albumin-bound medications is increased.

A 25—30% decrease in serum pseudo cholinesterase activity is also present at term, but it rarely produces significant prolongation of NMB action.

Increased cholesterol gall stone formation(progesterone).

↑ Blood Volume ( up to 90ml/Kg) ↑ by 1000 – 1500 ml at term.

↑ Plasma Volume(45%) > ↑ RBC mass(30%)

Dilutional anemia & ↓ blood viscosity

Facilitates maternal & fetal exchange of respiratory gases,

nutrients & metabolites

↓ Impact of maternal blood loss at delivery

• Pregnancy leads to a hypercoagulable state, due to,

a) factors VII, VIII, X, XII ,IX ( only factor XI )

b) fibrinogen and FDP's

c) fibrinolytic activity - levels of plasminogen activators

d) antithrombin III

Probably a protective adaptation to lessen the risks associated with the acute haemorrhage that occurs at delivery.

Increased risk of thromboembolic disease (Post-Anaesthesia ambulation )

Leucocytosis up to 13,000/µL.

↑ ESR

10-20% ↓ in platelet count.(Mild thrombocytopenia not a contra-indication for neuraxial block).

Marked ↓ cell mediated immunity→ ↑ susceptibility to viral infection.

Pregnancy is Diabetogenic

Human Placental lactogen(HPL) → relative insulin resistance.

• Biochemically Starvation like state

↓ Blood Glucose & Amino Acid levels.

↑ Free Fatty Acids, Ketones & triglycerides.

To promote fetal growth.

Maternal Insulin Levels Steadily Rise During Pregnancy

↓

Secretion of HCG and elevated levels of estrogens promote

hypertrophy of the thyroid gland.

Hyperplasia of Pancreatic ß Cells occurs in response to

increased demand for insulin secretions.

↑ TBG (↑ T3 & ↑ T4 ) → Free T3, T4 & TSH remain

normal.

• Increased level of relaxin - Softening Of Cervix

- Relax Symphysis Pubis

- Pelvic Joints

- Chest Wall Changes

Increased risk of back pain(lax ligaments)

41

Utero-placental Circulation

At term: uterine blood flow is 10% of CO≈ 600 – 700 ml/min.

80% to placenta20% to myometrium

42

Due to maximum dilatation of uterine vasculature its auto regulation is lost

Uterine Blood Flow

Directly proportional to difference betweenuterine arterial and venous pressure.

Inversely proportional to uterinevascular resistance.

Uterine vasculature has 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-adrenergic drugs (e.g.Phenylephrine) havesimilar effects causing less fetal acidosis.

43

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.

♦ Hypertensive disorders→ generalized vasoconstriction.

♦ Labor.

♦ Oxytocin infusions.

♦ Extreme hypocapniaPaCO2 < 20 mmhg.

♦ Barbiturates &Propofol.

44

Placental transfer of anaesthetic agents

Placental transfer of drugs depends on:

1) Molecular weight : < 1000 Da cross easily.

2) Protein binding– inversely proportional

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.

45

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

Cross placenta freely

Inhalational Agents

Intravenous Agents:

Thiopental, ketamine & propofol

Limited fetal effects in usual induction doses

(drug distribution, metabolism & placental uptake)

Variable effects.Cross placenta freelyOpioids

Most significant respiratory depressant effectsMorphine

Significant respiratory depression peaking 1- 3 hr after administration.

Pethidine

Minimal effect if < 1µg/Kg.Fentanyl

Minimal effects on fetus.

The highly ionized property impedes placental transfer.

Muscle Relaxants

46

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 cholinesterase in the maternal circulation.

Summary

To illustrate how all these changes may affect anaesthetic management, lets imagine performing a general anaesthetic for caesarean section and list some key points

1) Careful attention to the assessment of the airway and any necessary preparation to deal with a potentially difficult airway in the pre operative period.

2)When positioning the patient on the table, remember to use either a left tilt of 15 – 30 degrees on the table or a wedge under the right buttock to minimize aorto-caval compression.

3)Venous access 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. Intubation may be difficult and so adjuncts for difficult intubation should be available.

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) 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.