physiological changes in pregnancy

Physiological Changes In Pregnancy

Physiological Changes In Pregnancy

DR.FATMA AL-DAMMAS

Changes In Pregnancy Changes In Pregnancy

Pregnancy brings about many physical changes.

These changes can be divided into 3 area –

Anatomical

Physiological

Biomechanical.

Physiological Changes In PregnancyPhysiological Changes In Pregnancy

1.Pregnancy produces profound physiological changes that alter the usual responses to Anesthesia

2.Unique challenges - two patients are cared for simultaneously

3.Failure to take care can be disastrous for one or both of them

1. What are physiological changes during labour ?1. What are physiological changes during labour ?

Average maximum physiological changes associated with Pregnancy

Parameter Change

NeurologicMAC (minimum alveolar concentration)


Parameter Change

NeurologicMAC (minimum alveolar concentration) - 40%

1.(MAC) progressively decreases during pregnancy—atterm, by as much as 40%—for all general anesthetic agents

2.MAC returns to normal by The third day after delivery.

NeurologicNeurologic

Changes in maternal hormonal and endogenous opiate levels have been impilcated.

Progesterone,increases at term ↑β-endorphin levels during labor &delivery . local anesthesia reduced’ as much as 30%.

Central Nervous System

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

• Possible causes include:

a. increased diffusion of LA to the receptor site

b. increased sensitivity of nerve fibres to LA (Lower connection needed)

c. ? raised CSF progesterone levels

• Spinal ligaments including ligament flavum SOFT

Central Nervous System

• Valsalva manoeuvres during delivery may increase CSF and epidural pressures, markedly increasing the spinal spread of anaesthetia

2. What are Respiratory physiological changes during labour ?

2. What are Respiratory physiological changes during labour ?


Respiratory Oxygen consumption Minute ventilation Tidal volume Respiratory rate PaO2 PaCO2 HCO3 FRC (functional residual capacity)


Respiratory Oxygen consumption + 20 to 50%Minute ventilation Tidal volume Respiratory rate PaO2 PaCO2 HCO3 FRC (functional residual capacity)


Respiratory Oxygen consumption + 20 to 50%Minute ventilation + 50%Tidal volume Respiratory rate PaO2 PaCO2 HCO3 FRC (functional residual capacity)


Respiratory Oxygen consumption + 20 to 50%Minute ventilation + 50%Tidal volume + 40%Respiratory rate PaO2 PaCO2 HCO3 FRC (functional residual capacity)


Respiratory Oxygen consumption + 20 to 50%Minute ventilation + 50%Tidal volume + 40%Respiratory rate + 15%PaO2 PaCO2 HCO3 FRC (functional residual capacity)


Respiratory Oxygen consumption + 20 to 50%Minute ventilation + 50%Tidal volume + 40%Respiratory rate + 15%PaO2 + 10%PaCO2 HCO3 FRC (functional residual capacity)


Respiratory Oxygen consumption + 20 to 50%Minute ventilation + 50%Tidal volume + 40%Respiratory rate + 15%PaO2 + 10%PaCO2 - 15%HCO3 FRC (functional residual capacity)


Respiratory Oxygen consumption + 20 to 50%Minute ventilation + 50%Tidal volume + 40%Respiratory rate + 15%PaO2 + 10%PaCO2 - 15%HCO3 - 15%FRC (functional residual capacity)


Respiratory Oxygen consumption + 20 to 50%Minute ventilation + 50%Tidal volume + 40%Respiratory rate + 15%PaO2 + 10%PaCO2 - 15%HCO3 - 15%FRC (functional residual capacity) - 20%

Respiratory Effects Respiratory Effects

• Oxygen consumption and minute ventilation progressively increase during pregnancy.

• Both tidal volume and, respiratory rate increase. • By term, oxygen consumption has increased about 20

—40%, while minute ventilation has increased 40—50%.

• Paco2 decreases to 28—32 mm Hg; significant respiratory alkalosis is prevented by a compensatory ↓in pasma bicarbonate concentration.

Respiratory EffectsRespiratory Effects

• Hyperventilation may also increase Pa02 • Elevated levels o 2,3-di phosphoglycerate offset the

effect hyperventilation on hemoglobin affinity for oxygen.

• The P-50 for hemoglobin increases from 27 to 30 mm Hg the combination of these factors with increase in cardiac output enhances oxygen delivery to tissues.


The maternal respiratory pattern changes as the uterus enlarges.

• In the third trimester, elevation of diaphragm is compensated by an increase in the AP diameter of the chest

• Thoracic breathing is favored over abdominal breathing.

• Both vital capacity and closing capacity are minimally affected.

• FRC decreases up t 20° at term; FRC returns to normal within 48 hours of delivery.

• Reduction in expiratory reserve volume .


• Flow-volume loops are unaffected• Airway resistance decrease.• Physiologic dead space decreases but intrapulmonary

shunting increases towards term.• A chest film often shows prominent vascular markings

due to increased pulmonary blood volume and an elevated diaphragm.

• Pulmonary vasodilataion prevents pulmonary pressures form rising.

Respiratory: Importance for Anaesthesia

Respiratory: Importance for AnaesthesiaRespiratory: Importance for Anaesthesia

• ++Decreased FRC and increased oxygen consumption promotes rapid oxygen desaturation during periods of apnea .

• Preoxygenation prior to induction of general anesthesia is therefore mandatory to avoid hypoxemia in pregnant patients.

Following adequate preoxygenation, the PaO2 in apnoeic pregnant women falls

~ 80 mmHg/min more than in the nonpregnant state


• Closing volume exceeds FRC in up to half of all pregnant women when they are supine at term.

atelectasis hypoxemia.

• Parturients should not lie flat without supplemental oxygen.


Rapid gaseous induction

• ↓MAC (as much as 40% decreases at term return to normal on third day of delivery)

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

• ↓FRC ® less dilution• ↑MV ® rapid d depth


Intubation - Trauma- mucosal bleeding - difficult intubation• Capillary engorgement of the respiratory mucosa

during pregnancy predisposes the upper airways to trauma, bleeding, and obstruction.

• Gentle laryngoacopy and the use of small endotracheal tubes (6—7 mm) during general anesthesia.

Alteration of Lung Volume in Pregnancy

Functional Residual Capacity FVR

Residual Volume RV ~ 20% decrease

Expiratory Reserve Volume ERV

Vital Capacity VR

Inspiratory Reserve Volume IRV unchanged

Closing Volume CV

Total Lung Capacity TLC ~ 5% decrease

Inspiratory Capacity IC ~ 5% increase

3. What are Cardiovascular changes during labour ?


Parameter Change

Cardiovascular

Blood volume

Plasma volume

Cardiac output

Stroke volume

Heart rate

Peripheral resistance


Parameter Change

Cardiovascular

Blood volume + 35%

Plasma volume

Cardiac output

Stroke volume

Heart rate



Parameter Change

Cardiovascular

Blood volume + 35%

Plasma volume + 45%

Cardiac output

Stroke volume

Heart rate



Parameter Change

Cardiovascular

Blood volume + 35%

Plasma volume + 45%

Cardiac output + 40%

Stroke volume

Heart rate



Parameter Change

Cardiovascular

Blood volume + 35%

Plasma volume + 45%


Stroke volume + 30%

Heart rate



Parameter Change

Cardiovascular

Blood volume + 35%

Plasma volume + 45%


Stroke volume + 30%

Heart rate + 15 to 30%



Parameter Change

Cardiovascular

Blood volume + 35%

Plasma volume + 45%


Stroke volume + 30%

Heart rate + 15 to 30%

Peripheral resistance - 15%

Cardiovascular EffectsCardiovascular Effects

• Cardiac output and blood volume increase to meet accelerated maternal and fetal metabolic demands.

• An increase in plasma volume in excess of an increase in red cell mass produces dilutional anemia and reduce blood viscosity.

• Hemoglobin concentration remains greater than11.1gIdL.

• ↓in systemic vascular resistance by the second trimester decreases both diastolic and, to a lesser degree, systolic blood pressure.

• The response to adrenergic agents and

vasoconstrictors is blunted.


• 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.

• total blood volume reaches 90 mL/kg. • Average blood loss during vaginal delivery is 400—500 mL cesarean section 800—1000 mL

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


• ↑cardiac output (40% at term) is due to ↑in HR(15—30%) + SV (30%).

• Cardiac chambers enlarge and myocardial hypertrophy is often noted on echocardiography.

• Pulmonary artery, central venous, and pulmonary artery wedge pressures remain unchanged.

• Most of these effects are observed in the first and, to a lesser extent, the second trimester.


• In the third trimester, cardiac output does not appreciably rise, except during labor.

• The greatest increases in cardiac output are seen during labor and immediately after delivery.

• Cardiac output often does not return to normal until 2 weeks after delivery.

Blood Pressurea. CO ~ 50%

b. TPR - uterine AV shunt & decreased viscosity

slight decrease in MAP

NB: a high BP in pregnancy, except during labour, is always abnormal

• CVP and PAOP remain normal during pregnancy

• CVP increases 4-6 cmH2O during contractions

CVS: Importance for AnaesthesiaCVS: Importance for Anaesthesia

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

decreases of venous return to the heart as the enlarging uterus compresses the inferior vena cava.

• Up to 20% of women at term develop the supine hypotension syndrome.

(hypotension associated with pallor, sweating, or nausea and vomiting).


• It is due to complete or near-complete occlusion of the inferior cava by the gravid uterus.

• Turning the patient on her side typically restores venous return from the lower body and corrects the hypotension .


• The gravid uterus also compresses the aorta in pareurients when they are supine. ↓blood flow to the lower extremities and, more importantly, to the uteroplacental circulation.


• When combined with the hypotensive effects of regional or general anesthesia, aortocaval compression can readily produce fetal asphyxia.

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

• This maneuver is most readily accomplished by placing

a wedge (> 15 degrees) under the right hip.

• Chronic partial caval obstruction in the third trimester predisposes to venous stasis, phlebitis, and edema in the lower extremities.

Cardiovascular: Importance for Anaesthesia

• Patients undergoing spinal or epidural anaesthesia must,

a. Be maintained in a lateral tilt position, with left uterine displacement

b. Be adequately volume preloaded


• Elevation of the diaphragm shifts the heart’s position in

the chest, resulting in the appearance of an enlarged heart on a plain chest film

• left axis deviation and T wave changes on the ECG.

• Physical examination often reveals a systolic ejection flow murmur (grade I or II)

exaggerated splitting of the1ST heart sound (S1) third heart sound (S3) may be audible.

• A few patients develop small, asymptomaic pericardial effusions.

What are the criteria to diagnose cardiac disease during 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 arrythmias, atrial fibrillation or flutter

4. What are Renal changes during labour ?


Parameter Change

RenalGFR


Parameter Change

RenalGFR + 50%

Renal EffectsRenal Effects

• Renal vasodilatation increases renal blood flow early during pregnancy

• Autoregulation is preserved. • The kidneys often enlarge. • Increased renin and aldosterone levels promote sodium

retention. • Renal plasma flow and the glomerular filtration rate

increase as much as 50% during the first trirnester

Renal EffectsRenal Effects

• glomerular filtration declines toward normal in the third

trimester. • Serum creatinine and blood urea nitrogen decrease to

0.5—0.6 mg/dL and 8—9 mgldL• decreased renal tubular threshold for glucose and

amino acids results in : mild glycosuria (1—10 g/d)

prneteinuria (< 300 mg/d).• Plasma osmolality decreases by 8—10 mOsm/kg.

5. What are Gastrointestinal changes during labour ?

Gastrointestinal changesGastrointestinal changes

• Gastroesophageal reflux esophagitis are common during pregnancy.

• Upward and anterior displacemenr of the stomach by the uterus promotes incompetence of the gastroesophageal sphincter.

• Elevated progesterone levels reduce the tone of the gastroesophageal sphincter .

• Placental gastrin secretion causes hypersecretion of gastric acid.

• Intragastric pressure is unchanged.

Gastrointestinal changesGastrointestinal changes

increased risk of severe aspiration pneumonitis Gastric PH ≤ 2.5 Gastric volumes graeter than 25 ml≤60%. Delayed gastric emptying time Narcotics and anticholinergics reduce lower

esophageal sphincter pressure

6. What are hepatic changes during labour ?

Hepatic effecctsHepatic effeccts

• hepatic function and blood flow are unchanged• minor elevations in serum trarsaminases and lactic

dehydrogenase levels in the third trimester. • Elevations in serum alkalin phosphatase are due to its

seccetion by placenta .• A mild decrease in serum albumin is due to an

expanded plasma volume

• Colloid osmotic pressure progressively decreases, parallel with the fall in serum albumin


• A 25—30% decrease in serum pseudocholinescerase activity is also present at term

• rarely produces significant prolongation of succinylcholine’s action.

• The breakdown of mivacurium and ester-type local anaesthesia.

• Pseudocholinesrerase activity may not return to normal until up to 6 weeks postpartum.


• High progesterone levels appear to inhibit the release of cholecystokinin incomplete emptying of the gallbladder

altered bile acid composition, can predispose to formation of cholesterol gallstones.

6. What are hematological changes during labour ?


Parameter Change

HematologicHemoglobin

Platelets

Clotting factors


Parameter Change

HematologicHemoglobin - 20%

Platelets

Clotting factors


Parameter Change


Platelets - 10 to 20%

Clotting factors


Parameter Change


Platelets - 10 to 20%

Clotting factors + 50 to 250%

• Pregnancy leads to a hypercoagulable state, due to,

a. factors VII, VIII, X, XII (? IX)

b. fibrinogen and FDP's

c. fibrinolytic activity - levels of plasminogen activators

d. antithrombin III

increased risk of thromboembolic disease

e. W.B.C to 21000/cmm

f. Platelets by 10-20 %

7. What are metabolic changes during labour ?

Metabolic Changes

• Resemble starvation (blood glucose & aminoacidoses FFA, triglycerides & ketones

Favour fetal growth • Diabetogenic state• Insulin steadily • Relative insulin resistance(hCPL)• Pancreatic B-cell hyperplasia• Increased level of relaxin - softening Cx

- symphysis pubis

- pelvic joints

- ↑in back injury

Metabolic Changes

• Secretion of human chorionic gonadotropin and elevated levels of estrogens promote hypertrophy of the thyroid gland

• increase thyroid-binding globulin • T4 and T3 levels are elevated, free T4, free T3 • thyrotropin (thyroidstimulatiflg hormone) remain normal

• Serum calcium levels decrease• ionized calcium concentration remains normal.

URETROPLACENTAL BLOOD FLOW

Uteroplacental Circulation

• 10% CO• 600-700ml/min pregnancy (50ml/min non pregnant uterus)• 80% of (10% or 600ml)normally supply the placenta• 20% Myometrium

• Dilation of uterious vasculature(no auto regulation)

Uterine Blood Flow (No auto regulation)

• Abundant a-adrenergic & b-receptors

• Not affected by resp. gas tension

• But extreme hypocapnia Pa CO2< 20mmHg

• Proportional to uterine arterial and venous pressures

• Inversely proportional uterine vascular resistance


Factors affecting ↓UBF

• Systemic hypotension

• Uterine vasoconstriction

• Uterine contraction

• Aortocaval compression

• Hypovolemia


Factors affecting

• Systemic blockade(local blocks)

• Stress of labour (endogenous catacholamines)

• Phenylphrine (a-agonist)

N.B. Ephidrine mainly b-agonist (used in spinal and epi hypotension)

• Oxytocin & hypertonic contrations

PLACENTAL FUNCTION

Foetal functions Foetus depends on the placenta for

1.Gas exchange – Respiration

2. Nutrition

3. Waste product elimination

PHYSIOLOGIC ANATOMY PHYSIOLOGIC ANATOMY

• The placenta is composed of projections of fetal tissue (villi) that lie in maternal vascular spaces (intervillous spaces).

• As a result of this arrangement, the fetal capillaries within villi readily exchange substances with the maternal blood that bathes them.

PHYSIOLOGIC ANATOMY PHYSIOLOGIC ANATOMY

• Maternal blood in the intervillous spaces is derived from spiral branches of the uterine artery and drains into the uterine veins.

• Fetal blood within villi is derived from umbilical cord via two umbilical arteries and returns to the fetus via a single umbilical vein.

PLACENTAL EXCHANGE PLACENTAL EXCHANGE

Mechanssms of Placental exchange: 1. DIFFUTION Respiratory gases and small ions are transported by

diffusion. Most drugs used in anesthesia have molecular weights

well under 1000 can diffuse across the placenta.

2.BULK FLOW Water moves across by bulk flow.

3.ACTIVE TRANSPORT Amino acids, vitamins, and some ions (calcium and

iron) utilize this mechanism.

PLACENTAL EXCHANGE PLACENTAL EXCHANGE

Mechanssms of Placental exchange:

4.PINOCYTOSIS

large molecules, such as immunoglobulins, are transported by pinocytosis.

5.Breaks

Breaks in the placental membrane and mixing of maternal and fetal blood are probably responsible Rh sensitisation.

Respiratory Gas ExchangeRespiratory Gas Exchange

• oxygen has the lowest storage to utilization ratio. • term, fetal consumption averages about 21 mL/min• Fetal oxygen stores are normally 42 mL.• The normal fetus at term can survive 10 minutes or

longer .


• Transfer of oxygen across the placenta is dependent on the ratio of maternal uterine blood flow to fetal umbilical blood flow.

• The reserve for oxygen transfer is small. • PaO, of only 40 mm Hg. • The fetal hemoglobin oxygen dissociation curve

is shifted to the left such that fetal hemoglobin has greater affinity for oxygen than does maternal hemogloin


• fetal hemoglobin concentration is usually 15 g/dL (compared with approximately 12 g/d.L in the mother.

• Carbon dioxide readily diffuses across the placenta.• Maternal hyperventilation increases the gradient for

the transfer of carbon dioxide from the fetus into the maternal circulation.

• Fetal hemoglobin also appears to have less affinity for carbon dioxide than does maternal hemoglobin.

THE PHYSIOLOGY OF NORMAL LABOR

Stages of Labour

Effect of Labor on Maternal PhysiologyEffect of Labor on Maternal Physiology

• During intense painful contraction the minute ventilation increase up to 300%.

• Oxygen consumption increases 60% • excessive hyperventilation, PaCO2 ↓ below 20 mm Hg. • Excessive maternal hyperventilation reduces uterine

blood flow and promotes fetal acidosis.• analogous to an auto transfusion 300-500ml• Cardiac output rises 45% over third trimester values. • The greatest strain on the heart,occurs immediately

after delivery, 80% above prelabor values.

Pain pathways during labor

FETAL PHYSIOLOGY

FETAL PHYSIOLOGYFETAL PHYSIOLOGY• (1) Well-oxygenated blood from

the placenta (approximately 80% oxygen saturation) mixes with venous blood returning from the lower body(25% oxygen saturation) and flows via the inferior vena cava into the right atrium.

• 2. Right atrial anatomy preferentially directs blood flow from the inferior vena cava (67% oxygen saturation) through the foramen ovale into the left atrium.

• 3. Left aerial blood is then pumped by the left ventricle to the upper body (mainly the brain and the heart).

• 4. Poorly oxygenated blood from the upper body returns via the superior vena rays to the right atrium.

FETAL PHYSIOLOGYFETAL PHYSIOLOGY5. Right atrial anatomy preferentially

directs flow from the superior vena cava into the right ventricle.

6. Right ventricular blood is pumped into the pulmonary artery.

7. Because of high pulmonary vascular resistance,

95% of the blood ejected from the right ventricle

(60% oxygen saturation) is shunted across the ductus arteriosus, into the destending aorta, and

back to the placenta and lower body.

Obstetric Anaesthesia and its Challenges for the Anesthetist

Obstetric Anaesthesia and its Challenges for the Anaesthetist

• Obstetric anaesthetist must understand maternal adoption to pregnancy in order to manipulate physiological changes following general or regional anaesthesia and anaesthesia in such a way that the condition of the neonate at delivery is optimized

• Understanding Physiology of Pregnancy has enabled many more women with chronic diseases to achieve pregnancy

• Pharmokokinetics of anesthetic drugs during pregnancy

• Placental transfer of drugs


• Stress of multiple pregnancy, hypertension, PET, ET is well known now to anaesthetist. Distress of mother or fetus gives no leave way for anaesthetist but to conduct anaesthesia at VERY short notice without optimizing the condition

• Mother may be handling full stomach, bleeding, hypotension. Cannot be deferred otherwise we either loose mother or fetus or both

• Odd hours, emergency surgery without senior cover or at times lack of expert help culminates into catastrophic complications

• Maternal resuscitation, antepartum, postpartum hemorrhage etc.


• Neonatal resuscitation – another challenge for both anaesthetist and neontalogist

• Failure to intubation or ventilate and another night mare for anesthesia

• Sever bleeding intra-op with little or no help from blood bank in the form blood, platelets, factors may end into demise also

• Amniotic embolism an other dreaded complication of sudden collapse,DIC, and ARDS

• HELLP syndrome and associated organ problems in unplanned unforeseen patient could be too much demanding and stressful situation for the anesthetist


• Awareness during obstetric anaesthesia incidence is more than any other type of anaesthesia

• Supine hypotensive syndrome

• Epidural/ spinal failure/ collapse or cardiac arrest after spinal are some dreaded complications of obstetric anaesthesia

• Post spinal/ epidural headaches, backaches, quade-equina syndrome

Some Other Challenges in Obstetric Anaesthesia

• Anaesthesia during pregnancy for non-obstetric purpose e.g. appendectomy, cervical circulate, tocolytic therapy and its implication may end in abortion and pulmonary edema, ARDS, & CHF

• Fetal lung maturity in certain diseases - prematurity , diabetes etc

• Drug effects- induction at delivery time and placental transfer, fetal handling of drugs, implication on well being of the newborn

• Congenital anomalies – resuscitation or needing immediate surgery e.g. neural defects

Some Other Challenges in Obstetric AnaesthesiaTrauma in pregnancy - another challenge

• Sudden cardiac arrest and its management is quite different from other types of cardiac arrest

• Many challenging scenarios may happen - patient in lathotomy - head stuck - cervical tear - patient demoralized from bad conduct of labor & - an anesthetic called to help ???

• Drug abuse in parturient – another havoc

Obstetric Anaesthesia is a multidisciplinary team involving

• Obstetrician • Obstetric Anaesthetist • Midwife• Health visitors• Physicians• Neonatalogist

Therefore communication is of utmost importance and good record keeping is vital for obstetric anesthetist

“ A Pregnant Lady Is Like A Ticking Bomb That Can Burst Into

Fatality Any Moment” Channa A B

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