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Anaesthetic Management PHYSIOLOGICAL CHANGES IN PREGNANCY AND ITS

ANAESTHETIC IMPLICATIONS

Dr.J.Edward Johnson


PHYSIOLOGICAL CHANGES IN PREGNANCY AND ITS

ANAESTHETIC IMPLICATIONS

Determinants of uterine blood flow (UBF) in pregnant women:

UBF is directly proportional to the change in blood pressure across the organ

(mean arterial pressure minus central venous pressure) and inversely

proportional to uterine vascular resistance (UVR).

Flow = (UAP - UVP)/UVR,

where UAP is the uterine arterial pressure and UVP is the uterine venous

pressure. For example, during a contraction, uterine muscle tone increases,

increasing UVR and decreasing flow.

Autoregulatory curve for UBF:

UBF is not autoregulated but linearly proportional to mean arterial blood

pressure.

UBF affected by Uterine contractions during labour:

➢ UBF is approximately 700 mL/min at term.

➢ Approximately 70–90% of UBF passes through the intervillous space.

The uterine vascular bed is almost maximally dilated under normal conditions.

Uterine contractions decrease UBF secondary to increased UVP brought about by

increased intramural pressure of the uterus. There may also be a decrease in UAP

with contractions. Therefore, useful means of increasing UBF

✓ Correction of maternal hypotension

✓ Decrease of excessive uterine activity.

In the case of maternal hypertension, it is likely that the UVR is also increased.

This will result in decrease in UBF (according to the above equation). In the

preeclamptic patients, epidural analgesia increases the UBF and improves the

maternal blood pressure control during painful contractions.


Pressure over the Aorta proximal to the uterine artery as it passes over the brim

of the pelvis decreases the perfusion pressure of the uterine circulation and

hence decreases the utero-placental blood flow even in the absence of maternal

hypotension. This is again because there is no autoregulation of UBF.

Effects of regional anesthesia on UBF during labor:

• Regional anesthesia can increase UBF by reducing maternal pain and stress

during labor, which decreases uterine tone and vascular resistance.

• In contrast, hypotension caused by regional anesthesia can decrease UBF.

• In the setting of severe preeclampsia (PE), epidural anesthesia may increase

intervillous blood flow.

Epidural analgesia takes off the adrenergic response of labour pains. It is known

that increased levels of adrenaline/noradrenaline causes incoordinate uterine

contractions. So there will be no period where there is complete relaxation of the

uterine musculature allowing maximal UBF. Epidural breaks this vicious cycle and

the increases effective average UBF.

Effects of ketamine on UBF:

• Ketamine, in intravenous doses up to 1 mg/kg, is unlikely to alter UBF.

• Higher doses of ketamine (2 mg/kg) may decrease UBF due to increased

uterine tone (UVR)

• In case of decreased intravascular volume, ketamine may help to maintain

systemic blood pressure and thus maintain UBF.


Changes of CVS in Pregnancy:

Uterine blood flow increases gradually from 50 mL/min to 700 to 900 mL/min at

term with over 90% of the blood flow going to the intervillous space.

Normal ECG findings in pregnancy include

✓ Shortened PR

✓ Uncorrected QT interval

✓ A shift in the QRS axis in any direction

• A small right QRS axis deviation in the first trimester

• A small leftward QRS axis deviation in the third trimester

✓ Transient S–T segment changes.

✓ The most common benign dysrhythmias in pregnancy are premature

ectopic atrial and ventricular contractions and sinus tachycardia.

Systemic vascular resistance decreases from approximately 1,530 dyn s/cm5 to

1,210 dyn s/cm5 during pregnancy by several mechanisms.


✓ The production of prostacyclin, a potent vasodilator, is increased during

pregnancy.

✓ Progesterone also has a vasodilator effect on vascular smooth muscle.

✓ There is decrease in vascular tone due to α- and β-receptor down-

regulation.

✓ The physiologic anemia of pregnancy results in a change in rheology

resulting in decreased blood viscosity and improved blood flow, which also

decreases afterload.

The low resistance placental circulation is in parallel with the systemic circulation.

The sum of two resistances in parallel is less than either alone, which serves to

decrease the afterload.

Pulmonary vascular resistance (PVR) is also reduced by approximately 30% during

pregnancy, presumably by similar mechanisms. This may have important

implications in a patient with a shunt due to a congenital cardiac lesion as the

balance between SVR and PVR may be disrupted during pregnancy.

Despite a general decrease in vascular tone, there is greater maternal

dependence on the sympathetic nervous system for maintenance of

hemodynamic stability during pregnancy. The effects of decreased vascular tone

are primarily observed on the venous capacitance system of the lower

extremities. These effects counteract the untoward effects of uterine

compression of the inferior vena cava on venous return. Parasympathetic

deactivation toward term is likely to contribute to increased heart rate and

cardiac output at rest.

Complex hormonal mediation results in depression of baroreflexes during

pregnancy, making pregnant women even more susceptible to hypotension.

Auscultation Examination in the Pregnant Patient:

✓ Accentuation of first heart sound (S1) and exaggerated splitting of the

mitral and tricuspid components

✓ Typical systolic ejection murmur

✓ Possible presence of third heart sound (S3) and fourth heart sound (S4); no

clinical significance

✓ Leftward displacement of point of maximal cardiac impulse


Supine hypotension syndrome:

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. The syndrome results

from a profound drop in venous return for which the cardiovascular system is not

able to compensate.

The extent of compression of the aorta and inferior vena cava by the gravid

uterus depends on positioning and gestational age. In the supine position, nearly

complete obstruction of the inferior vena cava is evident at term. Blood returns

from the lower extremities through the intraosseous, vertebral, paravertebral,

and epidural veins. However, this collateral venous return is less than would occur

through the inferior vena cava, resulting in a decrease in right atrial pressure.

Compression of the inferior vena cava occurs as early as 13 to 16 weeks’ gestation

and is evident from the 50% increase in femoral venous pressure observed when

these women assume the supine position. By term, femoral venous and lower

inferior vena caval pressures are approximately 2.5 times the nonpregnant

measurements in the supine position.

Aortic compression in supine position results in increased maternal blood

pressure measured in the upper extremity analogous to an aortic cross clamp. At

the same time, arterial hypotension is occurring in the lower extremities and

uterine arteries. This results in decreased uterine blood flow to the fetus and fetal

hypoxia. Therefore, even with normal upper extremity maternal blood pressure,

uteroplacental perfusion may be decreased in the supine position.

Even when maternal blood pressure is normal, uterine artery perfusion pressure

decreases in the supine position because of increases in uterine venous pressure.

Blood flow to the uterus is proportional to perfusion pressure, i.e., UAP-UVP.

Compression of the inferior vena cava affects uteroplacental perfusion resulting in

an overall decrease in perfusion.

At term, the left lateral decubitus position results in less enhancement of cardiac

sympathetic nervous system activity and less suppression of cardiac vagal activity

than the supine or right lateral decubitus position. Women who assume the


supine position at term gestation experience a 10% to 20% decline in stroke

volume and cardiac output, consistent with the fall in right atrial filling pressure.

Blood flow in the upper extremities is normal, whereas uterine blood flow

decreases by 20% and lower extremity blood flow decreases by 50%. The sitting

position has also been shown to result in aortocaval compression, with a decrease

in cardiac output of 10%.

Normal findings of pregnancy differentiated from those indicating

heart disease:

➢ Systolic murmur greater than grade III;

➢ Any diastolic murmur;

➢ Severe arrhythmias; and

➢ Unequivocal cardiac enlargement on radiographic examination

Anesthetic Significance of Cardiovascular Changes of pregnancy:

➢ Venodilation may the incidence of accidental epidural vein puncture.

➢ Healthy parturients will tolerate up to 1,500 mL blood loss; transfusion

rarely required (hemorrhage at delivery remains an important risk).

➢ High hemoglobin levels (>14) indicate low-volume state caused by

preeclampsia, hypertension, or inappropriate diuretics.

➢ Cardiac output remains high in first few hours postpartum; women with

cardiac or pulmonary disease remain at risk after delivery.

➢ Epidural block reduces cardiac work during labor and may be beneficial in

some cardiac disease states.

➢ Maternal blood pressure of <90–95 mm Hg during regional block should be

of concern because it may be associated with a proportional decrease in

uterine blood flow.

➢ ALWAYS AVOID AORTOC AVAL COMPRESSION: 70–80% of supine

parturients with a T4 sympathectomy develop significant hypotension.


Haematological changes of pregnancy: A. Blood Volume:

✓ Blood volume +45%

✓ Plasma volume +55%

✓ Red blood cell volume +20%

✓ Hemoglobin concentration (g/dL) 11.6

✓ Hematocrit 35.5%

The increase in plasma volume exceeds the increase in red blood cell volume,

resulting in the physiologic anemia of pregnancy.

The physiologic hypervolemia facilitates

✓ Delivery of nutrients to the fetus

✓ Protects the mother from hypotension

✓ Reduces the risks associated with hemorrhage at delivery.

✓ Decrease in blood viscosity (lower hematocrit) creates lower resistance to

blood flow, which may be an essential component of maintaining the

patency of the uteroplacental vascular bed.

✓ Maintain blood pressure in the presence of decreased vascular tone

The increase in plasma volume results from fetal and maternal hormone

production, and several systems may play a role.

✓ The maternal concentrations of estrogen and progesterone increase nearly

100-fold during pregnancy. Estrogens increase plasma renin activity,

enhancing renal sodium absorption and water retention via the renin-

angiotensin-aldosterone system.

✓ Fetal adrenal production of the estrogen precursor

dehydroepiandrosterone may be the underlying control mechanism.

Progesterone also enhances aldosterone production. These changes result

in marked increases in plasma renin activity and aldosterone level as well as

in retention of approximately 900 mEq of sodium and 7000 mL of total

body water.

✓ The concentration of plasma adrenomedullin, a potent vasodilating

peptide, increases during pregnancy and correlates significantly with blood

volume.


Red blood cell volume increases in response to elevated erythropoietin

concentration and the erythropoietic effects of progesterone, prolactin, and

placental lactogen.

B. Plasma Proteins:

➢ Plasma albumin concentration decreases from a nonpregnant range of

• 4.1-5.3 g/dL to 3.1-5.1 g/dL in the first trimester

• 2.6-4.5 g/dL in the second trimester

• 2.3-4.2 g/dL in the third trimester.

➢ The globulin level decreases by 10% in the first trimester and then increases

throughout the remainder of pregnancy to 10% above the prepregnancy

value at term.

➢ The albumin-globulin ratio decreases during pregnancy from 1.4 to 0.9

➢ The total plasma protein concentration decreases from 7.8 to 7.0 g/dL.

➢ Maternal colloid osmotic pressure decreases by approximately 5 mm Hg

during pregnancy.

➢ The plasma cholinesterase concentration falls by approximately 25% during

the first trimester and remains at that level until the end of pregnancy.

C. Coagulation:

Pregnancy is associated with enhanced platelet turnover, clotting, and fibrinolysis.

Thus, pregnancy represents a state of accelerated but compensated intravascular

coagulation.

Changes in Coagulation and Fibrinolytic Parameters at Term Gestation:

➢ INCREASED FACTOR CONCENTRATIONS

✓ Factor I (fibrinogen)

✓ Factor VII (proconvertin)

✓ Factor VIII (antihemophilic factor)

✓ Factor IX (Christmas factor

✓ Factor X (Stuart-Prower factor)

✓ Factor XII (Hageman factor)

➢ UNCHANGED FACTOR CONCENTRATIONS

✓ Factor II (prothrombin

✓ Factor V (proaccelerin)


➢ DECREASED FACTOR CONCENTRATIONS

✓ Factor XI (thromboplastin antecedent)

✓ Factor XIII (fibrin-stabilizing factor)

➢ OTHER PARAMETERS

✓ Prothrombin time: shortened 20%

✓ Partial thromboplastin time: shortened 20%

✓ Thromboelastography: hypercoagulable

✓ Fibrinopeptide A: increased

✓ Antithrombin III: decreased

✓ Platelet count: no change or decreased

✓ Fibrin degradation products: increased

✓ Plasminogen: increased

✓ Increases in platelet factor 4 and beta-thromboglobulin signal

elevated platelet activation.

✓ Platelet aggregation in response to collagen, epinephrine, adenosine

diphosphate, and arachidonic acid is increased.

✓ The bleeding time measurement is not altered during normal

gestation.

✓ The platelet count usually decreases during the third trimester.

The most common causes of thrombocytopenia are

• Gestational thrombocytopenia,

• Hypertensive disorders of pregnancy, and

• Idiopathic thrombocytopenia.

The decrease in platelet count in the third trimester is due to increased

destruction and hemodilution. Gestational thrombocytopenia is an exaggerated

normal response.

Thromboelastrography demonstrates evidence of hypercoagulability in

pregnancy. These changes (decrease in R and K values, increase in the α angle and

maximum amplitude [MA], and decrease in lysis) are observed as early as 10 to 12

weeks’ gestation and are even greater during labor.


Anesthetic Significance of Hematologic Changes of pregnancy:

➢ A disproportionate increase in plasma volume to red blood cell volume

results in the “physiologic anemia of pregnancy.”

➢ In the absence of dietary iron supplementation, a hemoglobin

concentration of 11.6 gm/dl is typical.

➢ The increase in blood volume during pregnancy prepares the parturient for

normal blood loss at delivery. Blood loss is usually less than 500 Ml for

vaginal delivery and 1,000 mL for caesarean delivery.

➢ Hemodynamic changes due to blood loss are usually not observed until the

blood loss exceeds 1,500 mL and transfusion is rarely required unless blood

loss exceeds this amount.

➢ Normal pregnancy is associated with profound alterations in the

coagulation and fibrinolytic systems. Intrapartum blood loss is minimized

but risk of thromboembolism is increased.

➢ These changes are not detected by conventional tests (e.g., prothrombin

time, activated partial thromboplastin time).

➢ Most parturients have either a modest reduction (10%) or no change in

platelet count. A routine platelet count in the NORMAL parturient is

unnecessary prior to neuraxial anesthesia.

➢ If thrombocytopenia is suspected (e.g., preeclampsia, gestational

thrombocytopenia, idiopathic thrombocytopenic purpura), a platelet count

should be obtained in addition to assessment for clinical signs of bleeding.

Respiratory system changes of pregnancy:

✓ Tidal volume increases by nearly 45% during pregnancy.

✓ Progesterone acts as a direct respiratory stimulant and sensitizes central

respiratory centers, increasing the ventilatory response to CO2 and

producing a leftward shift of the CO2 curve.

✓ The hyperventilation of human pregnancy is the result of pregnancy-

induced changes in wakefulness and central chemoreflex drives for

breathing, acid–base balance, metabolic rate, and cerebral blood flow.

Although CO2 production at rest increases by about 300 mL/min during

pregnancy, a normal pregnant PaCO2 is 30 to 32 mm Hg, owing to the

hyperventilation.


✓ Due to increased urinary excretion of bicarbonate (normal pregnant level

20 mm Hg), however, pH is partially corrected normal pH is 7.41 to 7.44.;

✓ If a pregnant woman’s PaCO2 is 40 mm Hg, this indicates hypercarbia and

the need for further evaluation and treatment. each kilogram of maternal

tissue consumes oxygen at a rate of 4 mL/min, whereas the fetoplacental

unit and the growing uterus consume approximately 12 mL/min

Upper Airway Changes and Implications for Airway Management:

✓ Capillary engorgement of the larynx, nasal, and oropharyngeal mucosa

leads to increased mucosal friability and vascularity of the upper airway.

✓ Many patients complain of shortness of breath due to nasal congestion.

The hormonal influences of pregnancy and, in particular, the effects of estrogen

result in an increase in airway connective tissue, increased blood volume,

increased total body water, and an increase in interstitial fluid. These factors

contribute to hypervascularity and edema of oropharynx, nasopharynx, and

respiratory tract. All of these changes contribute to an increase in the Mallampati

classification of the airway during pregnancy and labor resulting in a

compromised airway. Pregnant women will typically require a smaller

endotracheal tube, usually 6.0 to 6.5 mm because of increased vascularity and


edema. Nasotracheal intubation and placement of nasogastric tubes should be

avoided unless absolutely necessary.

Thoracic Cage Changes during Pregnancy:

Increases in both the anteroposterior and transverse diameters contribute to a 5

to 7 cm circumferential enlargement of the thoracic cage. Increased levels of

relaxin causes structural changes in the ribcage resulting in relaxation of the

ligamentous attachment of the ribs. The diaphragm is elevated by as much as 4

cm, diaphragmatic excursion is increased.

Mechanisms of Hypoxemia in Pregnancy:

Hyperventilation causes decreased alveolar CO2 and leads to an increase in PaO2

(normal 103 to 107 mm Hg). By mid gestation, pregnant women often

demonstrate a PaO2 of less than 100 mm Hg.

In the supine position, FRC decreases further, and is exceeded by closing capacity.

This leads to

✓ Small airway closure

✓ An increase in ventilation/perfusion (V/Q) mismatch

✓ Decreased oxygen saturation.

Decreased cardiac output in the supine position will cause decreased mixed

venous saturation and therefore decreased arterial oxygen saturation.

Causes of Increased Oxygen Consumption during Pregnancy: Oxygen consumption

↑ by 40–60% during pregnancy as a result of:

➢ Increased metabolic needs of:

✓ Fetus

✓ Uterus

✓ Placenta

➢ Increased respiratory work

➢ Increased cardiac work

The authors found that after 99% denitrogenation, the time taken to decrease to

SaO2 <90% was 4 minutes in pregnant subjects and 7 minutes 25 seconds in

nonpregnant subjects. In addition, the time taken for SaO2 to fall to 40% from


90% was 35 seconds in pregnant subjects and 45 seconds in nonpregnant

subjects.

Reason for dyspnoea in pregnancy:

Dyspnea is a common complaint during pregnancy, affecting up to 75% of

women. Contributing factors include

✓ Increased respiratory drive

✓ Decreased Paco2

✓ The enlarging uterus

✓ Larger pulmonary blood volume

✓ Anemia and

✓ Nasal congestion.

Dyspnea typically begins in the first or second trimester but improves as the

pregnancy progresses. The hypoxic ventilatory response is increased during

pregnancy to twice the normal level, secondary to elevations in estrogen and

progesterone levels.

pH changes in pregnancy:

Metabolic compensation for the respiratory alkalosis of pregnancy reduces serum

bicarbonate concentration to approximately 20 mEq/L, the base excess by 2 to 3

mEq/L, and the total buffer base by approximately 5 mEq/L. This compensation is

incomplete, as demonstrated by the elevation of venous, capillary, and arterial

blood pH by 0.02 to 0.06 units.

Anesthetic Significance of Respiratory Changes in pregnancy:

➢ Airway management is more challenging:

✓ Weight gain and breast engorgement hinder laryngoscopy

✓ Swollen mucosa bleeds easily; avoid intranasal manipulation

✓ Use smaller endotracheal tube (6–7 mm)

➢ Response to anesthetics:

✓ MAC decreased

✓ Decreased FRC results in faster induction with insoluble agents

✓ Increased VE (expired volume) speeds induction with soluble agents

✓ Overdose with loss of airway reflexes may occur more rapidly


➢ Greater risk of hypoxemia:

✓ Decreased FRC causes less oxygen reserve during periods of apnea

✓ Increased oxygen consumption

✓ Rapid airway obstruction

➢ Excessive mechanical hyperventilation (PETCO2 <24) may reduce maternal

cardiac output and uterine blood flow.

➢ Maternal and fetal hypoxemia is associated with pain-induced hyper- and

hypoventilation. Effective analgesia avoids these changes.

Anesthetic Significance of Nervous System Changes in pregnanacy:

➢ Anesthetic requirements as measured by minimal alveolar concentration

(MAC), are decreased by as much as 30% from the nonpregnant state.

➢ More rapid uptake of volatile anesthetics occurs due to decreased FRC and

more rapid FA/FI rate of rise.

➢ These changes are significant because inhaled concentrations of

anesthetics that would be appropriate in a nonpregnant patient might

have exaggerated effects in the pregnant patient.

➢ A similar increased sensitivity to intravenous induction (e.g., propofol) and

sedative (e.g., benzodiazepines) agents is also seen.

➢ Neuraxial anesthetic requirements are decreased by approximately 40% at

term. Both biochemical and mechanical changes are responsible for the

decrease.

➢ Increased neuronal sensitivity to local anesthetics results in decreased

dose requirements for neuraxial anesthetics as early as the end of the first

trimester suggesting a biochemical or hormonal mechanism.

➢ Aortocaval compression results in epidural venous engorgement. This

decreases the volume of the epidural space, and the volume of CSF per

spinal segment.

➢ For a given dose of epidural or intrathecal local anesthetic, there will be a

greater degree of dermatomal spread.


Anesthetic implications of maternal physiologic changes in Neuraxial

Anesthesia:

Neuraxial anesthetic requirements are decreased by approximately 40% at term.

Two mechanisms are thought to be responsible for these changes:

➢ Pregnancy produces compression of the inferior vena cava resulting in

distension of the epidural venous plexus by the enlarging uterus;

➢ The volume of epidural fat increases and contributes to a further reduction

in subarachnoid cerebral spinal fluid (CSF) volume.

These mechanical changes produce decreases in the volume of the epidural

space, and also the volume of CSF per spinal segment. Thus, a given dose of

epidural or intrathecal local anesthetic will produce a greater degree of

dermatomal spread.

The decreased dose requirements for neuraxial anesthesia occur as early as the

end of the first trimester, long before significant epidural venous distension

occurs. This suggests that a biochemical or hormonal mechanism may be at work.

➢ The chronic exposure to progesterone causes alterations of receptor

activity, modulation of sodium channels, or altered permeability within

neuronal membranes leading to increased sensitivity to local anesthetics.

➢ In addition, decreases in CSF specific gravity and acid–base changes also

occur in the CSF. These factors may also influence the activity of local

anesthetics in the subarachnoid space.

Local anesthetic requirements for spinal anesthesia return to normal 8 to 24

hours postpartum.

TECHNICAL CONSIDERATIONS

✓ Lumbar lordosis increased

✓ Apex of thoracic kyphosis at higher level

✓ Head-down tilt when in lateral position

TREATMENT OF HYPOTENSION

✓ Decreased sensitivity to vasopressors


LOCAL ANESTHETIC DOSE REQUIREMENTS

✓ Subarachnoid dose reduced 25%

✓ Epidural dose unaltered or slightly reduced

Anesthetic Significance of Gastrointestinal Changes in pregnancy:

➢ Despite long-standing concern, ultrasound studies demonstrate that gastric

emptying remains normal throughout gestation, even in obese parturients. ➢ With the onset of painful contractions, however, gastric emptying is

slowed. Parenteral opioids have a similar effect. ➢ Neuraxial analgesia during labor has no impact on gastric emptying unless

fentanyl (or another opioid) is used to supplement the anesthetic. ➢ The consumption of clear liquids appears to promote gastric emptying.

Current ASA recommendations suggest that consumption of clear liquids by

laboring patients without additional risk factors (e.g., morbid obesity,

diabetes, difficult airway) is acceptable. ➢ Ectopic gastrin (secreted by the placenta) has the potential to increase both

the volume and acidity of gastric secretions. However, it has been shown by

a number of studies that plasma gastrin levels are reduced or unchanged

during pregnancy. ➢ Progesterone and estrogen relax the smooth muscle of the lower

esophageal sphincter (LES), decreasing the barrier pressure that normally

prevents gastroesophageal reflux. ➢ Elevation and rotation of the stomach by the enlarging uterus eliminates

the “pinch valve” at the entry point of the esophagus through the

diaphragm, further decreasing the barrier to reflux. ➢ Changes in LES tone increase both the risk of regurgitation and aspiration of

gastric contents, as well as the severity of the pulmonary injury that can be

expected after aspiration.


Anesthetic Significance of Hepatic Changes in pregnancy:

➢ Pregnancy induces reversible anatomic, physiologic, and functional changes

in the liver as a result of an increase in serum estrogen and progesterone.

➢ The amount of cardiac output distributed to the liver falls by 35% during

pregnancy despite systemic increases in blood volume and cardiac output.

➢ Pressure in the portal, and esophageal veins increases in the third trimester

due to pressure of the gravid uterus on the intra-abdominal venous system.

➢ These changes can be problematic if liver disease is present, since, for

example spider naevi and palmar erythema are signs of liver disease, but

may be seen in some pregnant women as a result of increased estrogen

levels.

➢ Telangiectasia and esophageal varices may appear in up to 60% of normal

pregnancies, without evidence of liver dysfunction. Care should be used in

placement of nasogastric tubes of esophageal temperature probes.

➢ Serum transaminases can be increased to the upper limits of normal. Liver

function tests are usually not affected by pregnancy except for the alkaline

phosphatase (ALP). Due to increased production of fetal and placental ALP,

maternal ALP can be increased up to 4 times normal which makes

interpretation of these laboratory results difficult.

➢ Average serum cholinesterase concentration is reduced by 24% before

delivery perhaps due to the large volume of distribution. The apneic

response to appropriate doses of succinylcholine is rarely prolonged.

Anesthetic Significance of Renal Changes in pregnancy:

➢ Alterations in the kidney and upper urinary tract are among the earliest and

most dramatic of the physiologic changes during pregnancy. Renal blood

flow increases by approximately 50–80% above prepregnancy levels.

Kidneys enlarge by up to 30%.

➢ Renal vasodilation results from increased levels of relaxin. Increases in

progesterone are responsible for dilation of the ureters and renal pelvis.

➢ The enlarged gravid uterus may obstruct the ureters leading to further

dilation of the ureters. Approximately 80% of women have hydronephrosis

by midpregnancy.


➢ The result of these anatomic alterations is an increased risk of urinary stasis

leading to infection and the potential for misinterpretation of diagnostic

imaging studies.

➢ Glomerular filtration rate and creatinine clearance are increased. Normal

values for creatinine and BUN during pregnancy are 0.5 mg/dL and 9

mg/dL.

➢ BUN and creatinine measurements that are normal or slightly elevated in

nonpregnant individuals indicate poor renal function during pregnancy.

➢ Increased GFR and tubular flow results in decreased proximal tubular

reabsorption and a physiologic glucosuria. Glucosuria is normal.

➢ Although proteinuria increases slightly and is due to the increased GFR,

reduced proximal tubular reabsorption and perhaps alteration in the

electrostatic charge of the glomerular filter, significant proteinuria is

abnormal

Anesthetic Significance of Endocrine Changes in pregnancy:

➢ Total T3 and T4 levels increase due to estrogen induced increases in thyroid

binding globulin. Free T3 and T4 remain unchanged during pregnancy.

➢ TSH levels decrease during the first trimester and return to normal levels

throughout the remainder of pregnancy.

➢ Pregnancy is associated with reduced tissue sensitivity to insulin. Pregnant

women will have higher blood glucose levels after a carbohydrate load.

➢ The fetal placental unit has a higher glucose consumption which results in

an altered response to fasting and exaggerated starvation ketosis.

➢ Hyperplasia of the lactotrophic cells in the pituitary results in a state of

hyperprolactinemia.

➢ Active cortisol levels are increased 2.5 times above nonpregnant levels and

result from increased production and decreased clearance of cortisol.

Anesthetic Significance of Musculoskeletal Changes in pregnancy:

➢ The enlarging uterus and weight gain place significant stress on the

musculoskeletal system due to shifts in the center of gravity of the body

that results in strain on the spine and pelvic joints.

➢ There is increased joint mobility during pregnancy secondary to the effects

of the hormone relaxin.


➢ Uterine growth results in significant lumbar lordosis, causing significant

strain on the lower back and increasing the risk of falls. Labor and

prolonged expulsive efforts also cause or exacerbate the back pain.

➢ Low back pain is the most common musculoskeletal complaint during

pregnancy and the puerperium.

➢ Although there has been long-standing concern about a causal relationship

between epidural anesthesia and development of long-term back pain,

prospective studies have consistently demonstrated a noncausal

relationship.

Effect do the Anaesthetic agents have on uterine tone:

➢ Volatile anesthetics: At 0.2 MAC minimal effect and beyond that dose-

dependent reduction in uterine tone. Below 1 MAC uterine response to

oxytocin is preserved.

➢ Local anesthetics (LA): Clinically insignificant effect at normal serum

concentration. Direct myometrial injection may cause uterine

hyperstimulation.

➢ Ketamine: Dose-dependent increase in uterine tone. Clinically insignificant

effect with normal induction dose.

➢ Opioids: No effect.

➢ Nondepolarizing NMBs: No effect on smooth muscle.

➢ Succinylcholine: No effect on smooth muscle.

Determinants of placental transfer:

➢ Maternal drug concentration

➢ Fetal drug concentration

➢ Placental factors (surface area, membrane thickness, and metabolism)

➢ Drug factors (lipid solubility, protein binding, molecular weight, and

ionization)

➢ Placental blood flow


Factors affecting the placental transfer of oxygen to the fetus:

Oxygen transfer across the placenta depends on the maternal-to-fetal blood

oxygen partial pressure gradient. There are several factors that affect transfer of

O2 to the fetus:

1. The parallel arrangement of maternal and fetal blood flow appears to have

a key role in human placenta.

2. The difference in oxyhemoglobin dissociation curves of maternal and fetal

blood: The fetal curve is positioned to the left of maternal curve and this

arrangement promotes transfer of oxygen across placenta.

3. The Bohr effect: The fetal-to-maternal transfer of carbon dioxide makes

maternal blood more acidic and fetal blood more alkalotic. This difference

causes right and left shifts of maternal and fetal O2 dissociation curves and

further enhances transplacental O2 transfer to the fetus.

P50 in the fetus and mother at term:

P50 is the partial pressure of O2 at which hemoglobin molecules are 50% saturated

with oxygen. P50 values are 19 and 30 mm Hg in the fetus and mother at term,

respectively. P50 is 27 mm Hg in normal adults.

Double Bohr and Double Haldane effect:

Both the Bohr and Haldane effects enhance the exchange of oxygen and carbon

dioxide across the placenta.

✓ The Bohr effect describes the shift of the hemoglobin dissociation curve to

the right by hydrogen ions, which reduces the affinity of hemoglobin for

oxygen.

✓ The Haldane effect describes the increased ability of deoxygenated blood

to carry more carbon dioxide.

The carbon dioxide from the fetal side diffuses into the maternal blood, causing

an increase in maternal intervillous hydrogen ion, which reduces the affinity of

maternal hemoglobin for oxygen, increasing oxygen transfer to the fetus.


At the same time, the relative decrease in carbon dioxide on the fetal side causes

the fetal blood to become slightly more alkaline, increasing the fetal hemoglobin

uptake of oxygen.

Since the Bohr effect occurs on both sides of oxygen delivery/uptake, it has been

called the double Bohr effect.

Likewise, the double Haldane effect describes maternal and fetal changes in

carbon dioxide and oxygen uptake. The fetal hemoglobin becomes oxygenated

and releases carbon dioxide, which has increased binding to the maternal

hemoglobin that has just deoxygenated.

The double Bohr effect occurs functionally by the slight opening and closing of the

hemoglobin chain allowing or blocking entry of oxygen to the iron-heme–binding

site. Carbon dioxide binding to the sentinel histidine on the hemoglobin chain can

block access of oxygen to the heme-binding site.


Reason for Fetal PaO2 is never more than 50–60 mm Hg even when

mother is on 100% oxygen:

This is due to several reasons:

➢ Placenta functions as a venous rather than arterial equilibrator. Because of

the shape of the O2 dissociation curve, maternal PaO2 above 100 mm Hg

does not provide significant increase in arterial O2 content.

➢ Placenta consumes a large amount of oxygen (20–30%) and this reduces

the amount of O2 available to transfer to the fetus.

➢ Fetal arterial blood represents a mixture of umbilical venous blood

(oxygenated) and inferior vena cava (IVC) blood (deoxygenated).

Normal PaCO2 in pregnancy:

About 30 mm Hg. Chronic mild hyperventilation is presumably a result of a

progesterone effect and causes increase in the TV and minute ventilation. The

PaCO2 declines to about 30 mm Hg by 12 weeks gestation and remains at that

level for the rest of the pregnancy.

Normal arterial blood gas (ABG) values in the parturient at term:

pH = 7.44, PaCO2= 30 mm Hg, PaO2= 103 mm Hg, and bicarbonate = 20 mEq/mL;

of course, the normal nonpregnant values are pH = 7.40, PaCO2 = 40 mm Hg,

PaO2 = 100 mm Hg, and bicarbonate = 24 mEq/mL. One can deduce that in the

parturient there is a respiratory alkalosis with metabolic compensation.

Maximal cardiac output in the parturient:

In the immediate postpartum period, cardiac output can increase up to 75%

above prelabor values.

“Autotransfusion” during labor:

Three hundred to 500 mL of blood will enter into the maternal circulation with

each uterine contraction during labor. This “autotransfusion” can increase cardiac

output and central blood volume by an additional 15–25%. When parturients

receive effective analgesia, cardiac output and stroke volume are augmented to a

lesser degree.


Critical period of organogenesis:

Between 15 and 60 days of gestation; however, the CNS does not fully develop

until after birth.

Factors affecting the placental transfer of thiopental administered to

the mother:

Following maternal administration, thiopental quickly appears in the umbilical

venous blood with mean F/M (Fetal: Maternal ratio) ratios between 0.4 and 1.1.

This suggests thiopental is freely diffusible. However, a wide intersubject

variability in umbilical cord blood concentration at delivery suggests factors other

than simple diffusion may play a role. Maternal and fetal protein concentration

strongly influences both maternal-to-fetal and fetal-to-maternal transfer of

thiopental.

Placental transfer rate of anticholinergics:

This directly correlates with the drugs’ ability to cross the blood–brain barrier.

Drugs such as atropine and scopolamine cross the placenta easily and have high

F/M ratios. Glycopyrrolate is poorly transferred, has a low F/M ratio, and

therefore does not result in fetal hemodynamic changes.

Inhalation induction of anesthesia faster in pregnant women than in

nonpregnant women:

➢ Decreased FRC and increased minute ventilation result in a more rapid rise

in alveolar concentration of anesthetic agent.

➢ Elevated cardiac output counteracts this effect somewhat, but the net

effect remains that of faster inhalational induction in pregnancy.

MAC of inhaled anesthetic agents in pregnancy:

MAC is reduced by 30% during early pregnancy and returns to normal within the

first 3 days following delivery.


Size of Endotracheal tube used in obstetric patients:

A 6.5 mm endotracheal tube is a good choice for most pregnant women. Small

size cuffed endotracheal tubes (6.0 –7.0 mm ID) should be available. Nasotracheal

intubation should be avoided and may lead to severe epistaxis.

Plasma cholinesterase activity change during pregnancy:

The plasma cholinesterase activity is reduced about 25%. After delivery there is a

further reduction to less than 60% of the nonpregnant value. However, there is no

clinically significant prolongation of action of succinylcholine or ester-type LA in

the dosages generally given.

Pain sensation difference between the first stage and the second

stage of labor:

During the first stage of labor, pain results from stretching of the uterus and

cervix. Pain signals are transmitted through visceral afferents to T10–L1 nerve

roots. This pain is often described as dull, aching, and cramping, and is poorly

localized. During the second stage of labor, pain results from stretching of the

vagina and perineum as the fetal head descends. This pain is transmitted through

somatosensory afferents to S2–S4 nerve roots and is described as sharp and well

localized.

Peripheral afferent or neuraxial block techniques to ameliorate pain

of the first stage of labor:

Amelioration of pain should occur with:

✓ Paracervical block

✓ Paravertebral sympathetic nerve block

✓ Epidural block from T10 to L1

✓ Intrathecal injection of an LA with or without opioid


Peripheral nerve block techniques (non-neuraxial) used during the

second stage of labor to provide analgesia:

Pudendal nerve block is an effective non-neuraxial technique for analgesia during

the second stage. It is not effective, however, for midforceps deliveries, uterine

manipulation, or repair of cervical lacerations. Paracervical and lumbar

sympathetic blocks provide analgesia only for the first stage of labor.

Major disadvantage of paracervical block:

Fetal bradycardia (up to 33%). It may be related to decreased UBF secondary to

uterine vasoconstriction from the LA applied closely to the uterine artery and

direct cardiac toxicity due to high fetal blood levels of LA

Relationship between the site of administration of LA drugs and

maternal peak blood levels:

For the various anesthetic techniques used in obstetrics, maternal peak blood

levels from highest to lowest are as follows: intravenous > intercostals > caudal >

paracervical block > epidural > subarachnoid block.

Placental transfer rate of LA:

LA agents readily cross the placenta. Fetal plasma protein binding is about 50%

that of maternal plasma. Therefore, at any given plasma concentration, there is

greater amount of free drug in the fetus than in the mother

LA distribution in fetal acidosis and hypoxemia:

The circulatory adaptation that results in increased blood flow to vital organs

causes higher concentration of LA in these organs than in healthy fetus.

“Ion trapping” of LA:

Decreased fetal pH will increase the concentration of ionized LA in the fetal

circulation. The ionization of the LA prevents diffusion across the placenta back to

the maternal circulation. The unionized LA continue to move to the fetus down its

concentration gradient. Thus, LA can accumulate in fetal blood. This phenomenon

is called “ion trapping” and explains the higher concentration of lidocaine in the

fetus in the presence of fetal acidosis.


LA used in epidural anesthesia and fetal distress:

2-Chloroprocaine (ester LA). It is fast in onset and rapidly hydrolyzed by the

mother and the fetus. Fetal acidosis less likely to promote fetal accumulation of

the LA.

Major disadvantages of using 2-chloroprocaine:

The duration of drug action is approximately 45 minutes, depending on the length

of the case, so the epidural may need to be topped up with a longer-acting LA.

Chloroprocaine may also antagonize the activity of neuraxial morphine used for

postoperative epidural analgesia.

Normal values for fetal blood gases:

In the fetus, the umbilical artery (UA) is traveling to the placenta. It therefore

carries with it the metabolic waste products of the fetus. Hence, it has low PaO2,

SpO2, and pH values, and high PaCO2 values. Conversely, the umbilical vein (UV) is

returning blood from the placenta. It therefore has higher values for PaO2, SpO2,

and pH, and low values for PCO2.

At birth normal fetal cord blood gas values are as follows.

➢ UV:

✓ pH 7.25–7.35

✓ PO2 28–32 mm Hg

✓ PCO2 40–50 mm Hg

✓ BE 0–5 mEq/L

➢ UA:

✓ pH 7.28

✓ PO2 16–20 mm Hg

✓ PCO2 40–50 mm Hg

✓ BE 0–10 mEq/L


Considerations for general anesthesia during pregnancy:

1. DRUGS:

➢ Propofol

✓ Induction dose decreased

✓ Elimination half-life unaltered

➢ Thiopental

✓ Induction dose decreased

✓ Elimination half-life prolonged

➢ Volatile anesthetic agents

✓ Minimum alveolar concentration (MAC) decreased, but unclear

whether hypnotic dose requirement differs from that in nonpregnant

women

✓ Speed of induction increased

➢ Succinylcholine

✓ Duration of blockade unaltered

➢ Rocuronium

✓ Increased sensitivity

➢ Chronotropic agents and vasopressors

✓ Decreased sensitivity

2. TRACHEAL INTUBATION:

➢ Increased rate of decline of PaO2 during apnea

➢ Smaller endotracheal tube required (6.5 or 7.0 mm)

➢ Increased risk of failed intubation with traditional laryngoscopy

➢ Increased risk of bleeding with nasal instrumentation


Ref:

1. STOELTING’S ANESTHESIA AND CO-EXISTING DISEASE, SEVENTH EDITION

2. CHESTNUT’S OBSTETRIC ANESTHESIA: PRINCIPLES AND PRACTICE, FIFTH

EDITION

3. Shnider and Levinson’s Anesthesia for Obstetrics F I F T H E D I T I O N

4. Anesthesiology BOARD REVIEW Third Edition

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