MODERATOR: DR.N.K. AGRAWALPRESENTED BY : DR. VISHAL KUMAR KANDHWAY

Effects of Anesthesia on Mother/Baby

Physiology

The average duration of human pregnancy: 280 days.

Uterine weight increases from 30gm to 1000gm.

As a result hormonal and major physiological adjustments occur to meet increasing demands of uterus, placenta and fetus.

Haematological

Maternal blood volume increases by approx 40% but plasma vol increases more than red cell vol – dilutional anaemia(Physiological anaemia).

These changes facilitate gas exchange with fetus and minimise the effects of blood loss at delivery.

Blood VolumeBlood Volume +40%+40%Plasma VolumePlasma Volume +45%+45%Red Cell volumeRed Cell volume +20%+20%White cell countWhite cell count IncreasesIncreasesHematocritHematocrit - 16%- 16%Plasma Proteins: AlbuminPlasma Proteins: Albumin -20%-20%αα1 1 αα2 2 ββ Globulin Globulin IncreasesIncreasesγγ Globulin Globulin DecreasesDecreasesFibrinogenFibrinogen +60%+60%ESRESR RisesRisesClotting factors 7, 8, 9, 10Clotting factors 7, 8, 9, 10 RisesRises

Plasma protein conc falls during pregnancy mainly due to 25% reduction in plasma albumin conc.

A:G ratio decreases. A substantial increase in fibrinogen - rise in

ESR.These alterations may affect the

pharmacokinetics of drugs.Particularly, changes in plasma protein conc

occur in pre-eclampsia.

Plasma cholinesterase is reduced in pregnancy- although its reduction is of clinical significance when Sch is used.

Coagulation: the rise in plasma fibrinogen is accompanied by increases in factors VII, VIII, IX, X.

Platelet count and adhesiveness probabaly remain unchanged although overall effect is one of hypercoagulability, and this may be related to production of DVT as well as being implicated in the etiology of preeclampsia and DIC.

Cardiovascular Changes in Pregnancy

  Parameter Change Amount (%) Heart rate Increased 20-30 Stroke vol Increased 20-50 C O Increased 30-50 Contractility Variable ±10 CVP Unchanged  PCWP Unchanged  SVR Decreased 20 BP Slight decrease Midtrimester

10-15 mmHg, then rises Pul vascular resistance Decreased 30 Pul artery pressure Slight decrease

The CVS changes are designed to serve two functions:

- To maintain normal utero-placental circulation.

- To facilitate the exchange of O2 ,CO2, nutrients and waste products between mother and fetus.

Anatomy - myocardium hypertrophy - displacement heart upwards ,

laterally and forwards and rotates it to a more transverse position.

HR = IncreasesBP = Systolic BP changes slightly, = DBP falls considerably in mid pregnancy,

then rises again during 3rd trimester.- Venous pressure - CVP is normal but rises when

measured with mother in supine (Pressure in lower limb veins is high in pregnancy and more so in supine position)

- Peripheral resistance is reduced in pregnancy and sympathetic blockade produced by regional anaesthesia may further decrease it.

Cardiac output rises substantially in early pregnancy and this elevation is sustained untill delivery.

Aortocaval compression

Compression of IVC upon vertebral bodies by the pregnant uterus when the mother lies supine, obstructs venous return.

Compensatory mechanisms act to increase peripheral vascular resistance and heart rate.

However few un-anaesthetised mothers experience hypotension and bradycardia when lying supine, and cardiac output may fall by 50%. This is revealed caval occlusion and result is SUPINE HYPOTENSIVE SYNDROME.

The aorta is also compressed by the uterus in supine position resulting in decreased femoral artery pressure. (no compensatory mechanism)

Aortocaval compression can cause;- Reduced uteroplacental blood flow- Decreased cardiac output- aortic compression- increased sympathetic tone causing fetal

hypoxia and acidosis

Anaesthetic Importance

The caval obstruction diverts blood flow to vertebral venous plexus, producing a relative decrease in volume of epidural space - lowered dose for epidural block.

POSEIRO effect:- reduction in pelvic perfusion and pulse pressure during uterine contraction in supine position enhancing the compressive effect of uterus on vertebral body.

Aortocaval compression renders CPR difficult in pregnant woman.

There can be aggravation of aortocaval compression following sympathetic blockade produced by central neuraxial blocks - strict avoidance of supine position and an adequate iv preloading are essential.

Respiratory

Anatomy:- Diaphragm is elevated- compensated for by

Increase in AP & transverse diameter of thoracic cavity (Hormonal relaxation of costal ligaments).

Capillary engorgement- higher chances of nasal bleed in nasal intubation.

Function:More susceptible to effects of apnoea due to--Increased O2 consumption-Increased Pulm ventilation-Decreased FRC

Anaesthetic Implication

Following rapid sequence induction- decreased FRC & increased O2 makes onset of hypoxemia very rapid.

Administer 100% O2 for 3 to 5 minutes while taking normal tidal breaths , or for four vital capacity breaths leads to effective nitrogen washout of FRC, such that maximal maternal oxygen reserves are attained before intubation.

The reduced FRC increases the rapidity of changes in the depth of anaesthesiawhile employing an inhaled anaesthetic technique.

MAC, of inhaled anaesthetic agent have been found to be decreased-may be due to progesterone.

GI Changes

Enhanced progesterone production may cause slower absorption of food.

Gastric secretions are more acidic and lower esophageal sphincter (LES) tone is decreased.

The risk of regurgitation on induction of general anesthesia depends, in part, on the gradient between the LES and intragastric pressures. In most patients, the gradient increases after succinylcholine administration because the increase in LES pressure exceeds the increase in intragastric pressure.

The efficacy of prophylactic nonparticulate antacids is diminished by inadequate mixing with gastric contents, improper timing of administration, and the tendency for antacids to increase gastric volume. Administration of histamine (H2) receptor antagonists, such as cimetidine and ranitidine, requires careful timing.

The administration of iv metoclopramide before elective cesarean section - hastens gastric emptying and increases resting LES tone in both nonpregnant and pregnant women.

A rapid-sequence induction of anesthesia, application of cricoid pressure, and intubation with a cuffed endotracheal tube are required for all pregnant women receiving general anesthesia.

Higher incidence of heart Burn - Lower esophageal sphincter tone and altered GE angle due to displaced diaphragm (not due to high abdominal pressure).

Heart Burn- should alarm against Increased risk of regurgitation during anaesthesia.

Anesthesia in 1st Trimester

Anesthesia during early gestation pose hazard to the developing fetus, by increasing the risk of congenital anomalies and spontaneous abortion.

In few studies an increased risk of hydrocephalus with other defects was found among offspring of mothers with reported first-trimester anesthesia

Anesthesia for Labour

Types : 1) GA 2) Regional anesthesia(spinal,

epidural or combined spinal and epidural).o In Emg. LSCS (cases with heavy/rapid

bleeding or other haemodynamic compromise), RA may not be appropriate & GA is preferred.

Regional Anesthesia

95% OF LSCS is preferred as it allows the mother to be awake and react immediately with her baby. The pain that is experienced because surgery is greater than that of labour and therefore requires a more intense nerve block.

The dermatomal level of anesthesia required for LSCS is also higher than that required for labour analgesia.

RA results in less neonatal exposure to drugs and provides better maternal post-op pain relief.

The potential for hypotension with this technique poses the greatest threat to the mother and baby.

The incidence of hypotension is similar between epidural and spinal anesthesia but occurs earlier and more rapidly with spinal approach.

The routine measures used to maintain uteroplacental perfusion and prevention of hypotension include pre-loading with IV fluids, lower leg compressive stockings & left lateral positioning.

GA

An important factor affecting neonatal outcome is the elapsed time between the induction of anesthesia and clamping of the umbilical cord, as this represents the time of fetal exposure to maternally administed medications.

A second factor is the time from uterine incision to delivery of the baby. A long incision to delivery time is associated with an increased incidence of fetal acidosis, caused by utero-placental vasoconstriction.

Induction agents used to initiate GA

Thiopental sodium : Following IV administration it rapidly reaches the brain and cause unconsciousness within 30-45 secs. At 1 min it reaches the peak conc. Of about 60% of the total dose in the brain, thereafter the drug distributes in the body and in 5-10 mins the conc. Is low enough such that consciousness returns.

It peaks in umbilical arterial plasma at 3-5 mins & declines rapidly in about 10 mins. Cord clamp within this times prevents neonatal depression.

Ketamine : tends to increase HR & BP. As it increases & maintain cardiac output, it is used in emg. LSCS when patients state of fluid volume is unknown.

Midazolam & Propofol are associated with longer induction time.

Effect of Anaesthetic Agents on Uterine activity and Labour

Inhalational Agents:-- Halothane, Isoflurane, Desflurane depress

uterine activity equally at equipotent doses; all causes dose dependent uterine relaxation.

- Higher doses can cause uterine atony and increased blood loss at delivery.

- Desflurane & Sevoflurane crosses the placenta easily resulting in depressed neonate. However once the neonate establishes ventilation, the lungs excrete these insoluble drugs more quickly.

Neuromuscular blocking agents

Scoline is degraded so rapidly by plasma cholinesterase that non reaches the fetus whereas few non-depolarising neuromuscular drug(rocuronium/pancuronium/atracurium) crosses the placenta and can reach the fetus.

Placental transfer of drugs

When passive diffusion is concerned placenta acts like lipid membrane, such as BBB. Hence , drugs which can cross BBB can also cross Placenta.

Inhalational agents cross placenta with ease.

Weak acids (barbiturates, narcotic analgesics, LA) all cross placenta readily in non-ionised state.

Fully ionised drugs(NMDA, other quarternary ammonium compounds) diffuse very slowly.

Placental Factors

The area of membraneMaternal and fetal blood flowPlacental enzymes

Placental Transfer of individual drugs

Inhalational anaesthetics:-- Diffuse rapidly.- The solubility of inhalational agents in

maternal and fetal blood is very similar.- The greatest disparity is seen with

halothane(1.3 times as slouble in maternal as in fetal blood).

Barbiturates;-weak acids whose pKa is near physiological

pH range.-are therefore largely non-ionised.-pass readily across placenta by lipid

diffusion.-protien binding is higher in maternal blood

thereforeat eqilibrium both free and total conc are higher in maternal blood.

Narcotic Analgesics:--are bases and are >95% ionised at

physiological pH.-nevertheless non-ionised fraction is of

sufficient lipid solubility for rapid placental transfer by lipid diffusion.

-pethidine can cause neonatal sedation with respiratory depression.

LA:--are weak bases and all cross placenta easily,

but their eqilibrium fetal-maternal ratios vary considerably.