Physiological changes in pregnancy & its anaesthetic implications
Dr. Swadheen kumar Rout1st year P.GDept. of AnaesthesiologyM.K.C.G College & hospital
INDIA -204 / 1,00,000 live births. USA - 7 / 1,00,000 live births. Although no studies in india, studies in usa haveshown that, 4-5% of total deaths are due to overzealous anaesthetic practices & its complications. So one must be familiar not only with the effect ofvarious drugs and techniques on the pregnant womenand foetus but also the physiological changes inpregnancy which alter response to anaesthesia.
Pregnancy produces profound physiologicalchanges(adaptive to stress) that become more significantas pregnancy progresses. 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 forsimultaneously , Failure to take care can be disastrous forone or both of them.
Fluid retention is the most fundamental systemic change ofnormal pregnancy. The total plasma volume is increased during pregnancy45%. The most marked expansion occurs in extra cellularvolume (ECV) with some increase in intra cellular water. The factors contributing – Increase sodium retention.(RAAS) Decrease in thirst threshold. Decrease in plasma oncotic pressure(↓ albumin)
At term, maternal blood volume has increased by1000—1500 mL in most women, allowing them toeasily tolerate the blood loss associated withdelivery.Normal delivery = 400-500ml blood lossCesarean section = 800-1000ml blood loss Blood volume does not return to normal until 1—2weeks after delivery
Cardiac output(40%) increases to meet accelerated maternal andfetal metabolic demands. This increase is mostly due to anincrease in stroke volume (30%) as heart rate increases onlyslightly (about 15%). Heart rate elevation occurs in response to increased oxygendemand. CO ↑ 40% by 12 weeks50% for rest of pregnancy60%-100% during labor & after delivery CO highest right after delivery (release of aorto-caval compression) dueto uterine contraction.
Peripheral vascular resistance (VR) decreases due tothe vaso-dilatory effects of progesterone and theproliferation of low resistance vascular beds in theinter-villous spaces of the placenta. Because of the decrease in peripheral vascularresistance(inspite of increased CO), arterial bloodpressure does not significantly change or may show aslight fall in a uncomplicated pregnancy. Diastolic(20%) > Systolic(8%) The response to adrenergic agents and vasoconstrictors isthus blunted.
Despite the increase in blood volume, there is nochange in the central venous pressure(CVP) duringpregnancy. This is likely due to dilated systemic andpulmonary circulations. Cardiac chambers enlarge and myocardial hypertrophy isoften noted on echocardiography.(eccentric due toactivation of RAAS). Also show variable ECG,ECHO,CXR Changes.
Effect of Pregnancy on Cardiovascular InvestigationsInvestigation FindingsChest radiography Apparent cardiomegalyEnlarged left atrium (lateral views)Increased vascular markingsStraightening of left-sided heart borderPostpartum pleural effusionECG Right-axis deviationRight bundle branch blockST-segment depression on left precordial leadsQ waves in lead IIIT-wave inversion in leads III, V2, and V3Rotation of 15 degrees(QRS axis)ECHO Trivial tricuspid regurgitationPulmonary 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 thicknessMitral regurgitation (28% at term)Pleural effusion (40% postpartum)From Gei AF, Hankins GDV: Cardiac disease and pregnancy.
Occurs in 20% of women at term.Aorto-caval compressionCompression of IVCCompression of lower aorta↓ COP by 24% at term.↓ blood flow to kidneys,utero-placental circulation &lower extremetiesSupine Hypotension syndrome(hypotension associated with pallor, sweating,or nausea and vomiting)Decreases in cardiac output can occur inthe supine position after the 28th week ofpregnancy.Fetal hypoxia
Women with a 28-week or longer gestation shouldnot be placed supine without left uterinedisplacement. Can be done byLeft lateral decubitusTilting the tableLeft side downRigid wedge (>15 degree)underThe right hipFluid preloading before neuro-axial anesthesiaIt does not completely avoid maternal hypotension butIt ↑ maternal COP → preserve utero-placentalblood flow.
Physical examination of the term pregnant womanmay also be abnormal with auscultation commonlyrevealing a wide, loud, split first heart sound, an S3sound, and a soft systolic ejection murmur. Hence essential to differentiate abnormalcardiovascular changes from normal physiologicalchanges 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 arrythmias, atrial fibrillation orflutter
Changes in the respiratory system during pregnancyinvolve the upper airways, minute ventilation, lungvolumes, and oxygen consumption. Major physiological changes occur in the respiratorysystem during pregnancy due to a combination of bothhormonal and mechanical factors. Dyspnoea is a common complaint in pregnancyaffecting over half of women at some stage.
Due to increased metabolic demands, Oxygenconsumption (+ 20 - 50%) and minute ventilation(+40- 50%) progressively increase during pregnancy.(Increased progesterone sensitizes the centralrespiratory center to carbon dioxide – directlystimulating ventilation) The pregnant woman thus takes larger Tidalvolumes(40-50%) to eliminate carbon dioxide. Paco2 decreases to(28—32 mm Hg); significantrespiratory alkalosis is prevented by a compensatory ↓in pasma HCO3 concentration.
Hyperventilation may also increase Pa02. Elevated levels of 2,3-diphosphoglycerate offsetthe effect of hyperventilation (↓PaCO2) onhemoglobin affinity for oxygen. The combination of increased 2,3-DPG withincrease in cardiac output enhances oxygendelivery to tissues.
The maternal respiratory pattern changes as theuterus enlargesDiaphragm rises up(4cm) compensatory increases inAntero-posterior diametersDiaphragm motion not restrictedChest wall limitationThoracic breathing favoured over Abdominal20% decrease in FUNCTIONAL RESIDUAL CAPACITY(FRC).* No change in CLOSING CAPACICITY (CC) & VITAL CAPACITY
Pregnant woman has a smaller “air tank”.Non-pregnantwoman
↓ FRC/CC + ↑O2 Consumption=Rapid O2 de-saturation duringperiods of apnea (diminished capacity totolerate apnea).Supine Position & Regional Blockfurther diminishes FRCPre-oxygenation prior to induction of generalanesthesia should be given to avoid hypoxemia inpregnant patients.Rapid devlopment of hypoxemia
Rapid gaseous induction The decrease in FRC coupled with the increase in minuteventilation accelerates the uptake of all inhalationalanesthetics. ↓FRC ® less dilution ↑MV ® rapid deep depth
Hormonal Changes Capillary engorgement ofrespiratory tract mucosa1) ↑ Incidence of difficult intubation.2) Trauma and bleeding duringendotracheal intubation.☼ Repeated attempts at laryngoscopy 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 normallevel at termβ- endorphin surge duringlabor & delivery
LA requirements for subarachnoid or epidural anaesthesiaare reduced in pregnancy (30%) a) ↑ diffusion of LA to the receptor site.b) ↑ sensitivity of nerve fibres to LA (Lower CONCN.needed).c) engorged epidural venous plexus.d) ? raised CSF progesterone levels. Spinal ligaments including ligament flavum SOFT henceloss of resistance technique used for regional block may bemaskedCNS : its anaesthetic importance
IVC obstruction by enlarginguterusEngorged EpiduralVenous Plexus1) ↓CSF Volume2) ↓Volume ofEpidural Space3) ↑Epidural spacePressure1,2: This enhances the cephalad spread of LAduring regional blocks.3 : Predisposes to higher incidence of dural puncture &intravascular injection
The parturient should be considered a full stomach patientduring most of gestation☼ Upward & ant. displacement of the stomach by theuterus → Incompetence of gastro-esophagealsphincter → 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 loweresophageal sphincter pressure (used with precaution)For GA:Pharmacological prophylaxis against aspiration.Supine position with lateral tiltNo positive pressure ventilation before intubationRapid sequence induction.Sellick’s maneuver
Renal vasodilatation increases renal blood flowearly during pregnancy. ↑ Cardiac output(CO) ↑ GFR & ↑ RPF(renalplasma flow) by 50%. ↑ Renin & Aldosterone level promotes Na+ retentionleading to volume overload. ↓ Renal tubular threshold for glucose & amino acids →mild glycosuria & proteinuria (< 300mg/d).
↑ GFR ↑ clearance of urea, uric acid andcreatinine↓ plasma concentrations ofsr. Creatinine & BUNBUN and Creatinine levels that would be consideredmarginally elevated in pre-pregnant patients are usuallyindicative of severe renal impairment in pregnancy.
Hepatic function and blood flow are unchanged. A mild ↓ in serum albumin is due to an expandedplasma volume. Thus, the free fraction of albumin-bound medications is increased. A 25—30% decrease in serum pseudocholinesteraseactivity is also present at term,but it rarely producessignificant prolongation of SCh action. Increased cholesterol gall stoneformation(progesterone).
↑ Blood Volume ( up to 90ml/Kg)↑ by 1000 – 1500 ml at term.↑ Plasma Volume(45%) > ↑ RBC mass(30%)Dilutional anemia & ↓ blood viscosityFacilitates maternal & fetalexchange of respiratory gases,nutrients & metabolites↓ Impact of maternal bloodloss at delivery
• Pregnancy leads to a hypercoagulable state, due to,a) factors VII, VIII, X, XII ,IX ( only factor XI )b) fibrinogen and FDPsc) fibrinolytic activity - levels of plasminogen activatorsd) antithrombin III Probably a protective adaptation to lessen the risksassociated with the acute haemorrhage that occurs atdelivery. Increased risk of thromboembolic disease (Post-Anaesthesiaambulation )
Leucocytosis up to 21,ooo/µL. ↑ ESR 10-20% ↓ in platelet count.(Mild thrombocytopenia not acontra-indication for neuraxial block). Marked ↓ cell mediated immunity→ ↑ susceptibility toviral infection.
Secretion of HCG and elevated levels of estrogenspromote hypertrophy of the thyroid gland. ↑ TBG (↑ T3 & ↑ T4) → Free T3, T4 & TSH remainnormal.
• Increased level of relaxin - softening cervix- relax symphysis pubis- & pelvic joints Increased risk of back pain(lax ligaments)
Utero-placental CirculationAt term: uterine bloodflow is 10% of CO≈ 600 – 700 ml/min.80% to placenta20% to myometrium
Maximally dilates uterine vasculature so autoregulation is absent.Uterine Blood FlowDirectly 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-adrenengic drugs (e.g.Phenylephrine) havesimilar effects causing less fetal acidosis.
Placental transfer of anaesthetic agentsPlacental transfer of drugs depends on:1) Molecular weight : < 500 Da cross easily.2) Protein binding– inversely proportional3) 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 givenand route of administration.6) Timing of administration.
Local anesthetics → Placental transfer depends on:1) pKa.2) Maternal & fetal pH : Fetal acidosis → higher fetal to maternaldrug ratios . Binding of hydrogen ions to the nonionized form → trappingof local anesthetic in fetal circulation3) Degree of protein binding : highly protein bound agentsdiffuse poorly across the placenta.Chloroprocaine has the least placental transfer as it is rapidlybroken down by plasma cholinestrase in the maternal circulation.
Effect of labor on maternal physiologyStages of labor1st stage 2nd stage 3rd stageStarts with true laborpains, ends by fullcervical dilation.Starts with full cervicaldilation, fetal descentoccurs, ends with completedelivery of fetus.Extends from birth of thebaby to delivery of theplacenta.Latent phase Active phaseProgressive cervical effacement& minor dilataton (2 – 4 cm).Progressive cervical dilatationup to 10 cm.8 – 12 h in nulliparous5 – 8 h in multiparous.Contractions are 1.5- 2 minapart, last 1 – 1.5 min15 – 120 min.15 – 30 min.
Intense painful contractionsMaternal hyperventilationMV ↑ up to 300%.↑ O2 consumption 60%above 3rd trimester valuesMarked HypocapniaPaCo2 < 20 mmHgUterine VasoConstriction(fetal acidosis)Periods of hypoventilation → transientmaternal & fetal hypoxemia in betweenContractions.
Each contractionDisplaces 300 – 500ml blood fromuterus to central circulation.COP ↑ 45% above 3rd trimesteric value.Maximum strain on the heart occurs immediatelyafter delivery.Uterine intense involution→ sudden relieve of IVC→ ↑ COP 80% above prelabor values.
SummaryTo illustrate how all these changes may affect anaestheticmanagement, lets imagine performing a general anaesthetic forcaesarean setion and list some key points1) Careful attention to the assessment of the airway and anynecessary preparation to deal with a potentially difficult airwayin the pre operative period.2)When positioning the patient on the table, remember to useeither a left tilt of between 15 – 30 degrees on the table or awedge under the right buttock to minimize aorto-cavalcompression.3)Venous access often easier due to engorgement of the venoussystem
4) Pre oxygenation is essential and should be with a tight fittingmask for at least 3 minutes.5) Rapid sequence induction with the application of cricoidpressure is mandatory. Intubation may be difficult and soadjuncts for difficult intubation should be available.6) Once the airway is secured, ventilation should be aimed tokeep 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 exogenouscatecholamines and so if vasopressors are required to maintainadequate blood pressure, the amounts needed may be greater.10) Extubation should be done with the patient awake and ontheir side to reduce the risk of aspiration of gastric contents.