PHYSIOLOGICAL CHANGES IN PREGNANCY

Presentation by : DR NIVEDITA

HAEMATOLOGICAL CHANGES

 HYPERVOLEMIA ASSCIATED WITH NORMAL PREGNANCY AVERAGES 40 TO 45 % ABOVE NON PREGNANT STATE IMPORTANT FUNCTIONS:
TO MEET THE METABOLIC DEMANDS OF ENLARGED UTERUS TO PROVIDE NUTRIENTS AND ELEMENTS TO GROWING FETUS AND PLACENTAE TO PROTECT MOTHER AND FETUS AGAINST DELETRIOUS EFFECT OF IMPAIRED VENOUS RETURN IN SUPINE AND ERECT POSITION TO SAFEGUARD MOTHER AGAINST THE ADVERSE EFFECT OF BLOOD LOSS ASSOCIATED WITH PARTURITION

BLOOD VOLUME EXPANSION OCCURS DUE TO INCREASE IN BOTH PLASMA AND ERYTHROCYTES ,MORE PLASMA THAN ERYTHROCYTES IS ADDED TO CIRCULATION

HB CONCENTRATION AND HAEMATOCRIT

DUE TO PLASMA AUGUMENTATION
HB CONCENTRATION AND HAEMATOCRIT DECREASE DURING PREGNANCY BLOOD VISCOCITY DECREASES

HB DECREASES TO 12.5G/DL TERM ,BELOW 11G/DL IS CONSIDERED ABNORMAL DUE TO IRON DEFICIENCY ANAEMIA.

IRON METABOLISM
TOTAL IRON CONTENT IS 2 TO 2.5 G (HALF OF THAT IN MAN) IRON STORES IS 300MG.

IRON REQUIREMENTS
1000 mg of iron is required for normal pregnancy -300mg for placenta and fetus, 200mg lost through excretion primarily through GI tract which is lost even when mother is anaemic. THE AVERAGE INCREASE IN CIRCULATORY VOLUME IS ABOUT 450ML ANOTHER 500MG IS NEEDED(1ML OF ERYTHR HAS 1.1MG OF IRON). MOST IRON IS USED DURING LATER HALF OF PREGNANCY WHEN IRON REQUIRMENT IS INCREASED TO 6 TO 7MG/DAY FOR WHICH MATERNAL SUPPLEMENTATION IS NEEDED WHICH IF NOT GIVEN HB AND HAEMATOCRIT FALLS AS BLOOD VOL INCREASES FETAL RED CELL PRODUCTION IS NOT IMPAIRED AS PLACENTA TRANSFERS IRON EVEN WHEN MOTHER HAS IRON DEFICIENCY ANAEMIA.

THE PEURPERIUM
AT THE TIME OF VAGINAL DELIVERY AND OVER NEXT FEW DAYS ONLY HALF OF THE ADDED ERYTHROCYTES ARE LOST, WHICH IS FRON PLACENTAL IMPLANTATION SITE, EPI SITE /LOCHIA. MATERNAL ERYTHROCYTES CORRESPONDING TO 500-600ML OF PREDELIVERY WHOLE BLOOD IS LOST.

IMMUNOLOGICAL FUNCTION
PREGNANCY IS ASSOCIATED WITH SUPPRESSION OF CELL MEDIATED AND HUMORAL IMMUNOLOGICAL FUNCTION TO ACCOMMODATE FOR SEMIALLOGENIC FETAL GRAFT. SUPPRESSION OF T HELPER CELL AND CYTOTOXIC T CELL WHICH LEADS TO DECREASED SECRETION OF INTERFERON GAMA, INTERLEUKIN 2 AND TUMOUR NECROTIC FACTOR BETA, SUPPRESSION OF TH1 IMMUNE RESPONSE IS PREREQUISITE FOR PREGNANCY CONTINUATION ----- ALSO EXPLAINS PREGNANCY RELATED REMMISSION OF CERTAIN AUTOIMMUNE L (RA,MS,AUTOIMMUNE THYROIDITS) FAILURE OF TH1 SUPPRESSION IS RELATED TO PREECLAMPSIA UPREGULATION OF TH2 CELL AND INCREASED SEC OF IL4,IL6,IL13,IgA AND IgG HIGHER IN PREG, AMOUNT OF INTERLEUKIN 1 BETA IS INCREASED IN CX MUCUS.

LEUKOCYTES OF RELAXIN
SOME POLYMORPHONUCLEAR LYMPHOCYTE FUNCTION LIKE CHEMOTAXIS, ADHERENCE IS DEPRESSED FROM SECOND TRIMESTER OF PREGNANCY WHICH IS THOUGHT TO BE DUE TO INHIBITORY EFFECT RELAXIN ON NEUTROPHIL ACTIVATION VALUE OF WBC---- 5000 TO 12000/MICROLIT MAST CELL PLAY IMP. ROLE IN UTERUS CONTRACTILITY DURING THE THIRD TRIMESTER --- GRANULOCYTES AND CD8 T LYMPHOCYTES INCREASED, CD4 REDUCED.

INFLAMMATORY MARKERS
LEUKOCYTE ALKALINE PHOSPHATASE IS ELEVATED. C4 WOMAN NOT IN LABOUR 1.5MG/DL. ESR ELEVATED IN DUE TO ELEVATED PLASMA GLOBULIN AND FIBRINOGEN. C3 & C4 ELEVATED.

COAGULATION AND FIBRINOLYSIS

BOTH COAGULATION AND FIBRINOLYSIS IS AUGUMENTED BUT REMAIN BALANCED TO MAINTAIN HAEMOSTASIS ENHANCED IN MULTIFETAL GESTATION INCREASED CONCENTRATION OF ALL CLOTTING FACTORS EXCEPT XI AND XIII. INCREASED LEVEL OF HIGH MOL WT FIBRINOGEN, PLASMA FIBRINOGEN (FACTOR I) IN NON PREGNANAT STATE 300 MG/DL. DURING NORMAL PREGNANACY INCREASES BY 50% I.E. 450 MG/DL THIS LEADS TO INCREASED ESR. tPA ACTIVITY GRADUALLY DECREASES OVER THE CORSE OF NORMAL PREGNANCY
tPA converts plasminogen to plasmin and causes fibrinolysisand produces FDP PAI INCREASES DURING PREGNANCY FIBRINOLYTIC ACTIVITY IS IMPAIRED ARE COUNTERED BY INCREASED LEVEL OF PLASMINOGEN AND DECREASED LEVEL OF ANOTHER PLASMINOGEN INHIBITOR ALPHA 2 ANTIPLASMIN WHICH ENSURES HAEMOSTASIS IN PREGNANCY

PLATELETS
AV COUNT IS DEC DURING PREGNANCY THROMBOCYPENIA IS DEFINED AS BELOW 2.5TH PERCENTILE (116000/ML)-DUE TO HAEMODILUTION,ALSO PLATELET CONSUMPTION INCREASES DUE TO INCREASED PRODUCTION OF THXA2

REGULATORY PROTIEN
THROMBOPHLIAS - INHERITED OR ACQUIRED DEFICIENCY OF PROTIEN C,S,Z AND ANTITHROMBIN RESPONSIBLE FOR THROMBOEMBOLIC EPISODE DURING PREGNANCY ACTIVATED PROTIEN C ALONG WITH PROTIENS AND FACTOR V FUNCTION AS ANTICOAGULANT BY NEUTRALIZING THE PROCOAGULANT VA AND VIIIA. BETWEEN THE FIRST AND THIRD TRIMESTER LEVEL OF ACTIVATED PROTIEN C AND S DECREASES. OCP DECREASES PROTIEN S. PROTIEN Z IS A VITAMIN K DEPENDANT GLYCOPROTIEN THAT INHIBITS ACTIVATION OF FACTOR X --- ASSOCIATED WITH RISK OF RECCURENT EARLY PREG LOSS LEVELS OF ANTITHROMBIN REMAINS CONSTANT

SPLEEN
BY THE END OF NORMAL PREGNANCY SPLENIC AREA ENLARGES BY 50%. THE ECHOGENIC APPEARANCE OF SPLEEN REMAINS HOMOGENOUS THROUGHOUT

GIT TRACT
AS PREGNANCY ADVANCES
THE STOMACH AND INTESTINE ARE DISPLACED BY ENLARGING UTERUS; APPENDIX IS DISPLACED UPWARD AND LATERALLY AS UT ENLARGES IT MAY REACH RT FLANK

GASTRIC EMPTYING TIME REMAINS UNCHANGED IN EACH TRIMESTER DURING LABOUR AND AFTER ADMINISTRING ANALGESICS GASTRIC EMPTYING TIME IS PROLONGED SO THERE IS MAJOR DANGER OF GASTRIC ASPIRATION. PYROSIS (HEART BURN) ----- COMMON DUE TO REFLUX OF ACIDIC SECRETIONS IN LOWER OESOPHAGUS ---- LES TONE IS DECREASED, INTRAGASTRIC PRESSURE IS HIGHER, OESOPHAGEAL PERISTALISIS HAS LOWER WAVE SPEED AND LOWER AMPLITUDE

GUMS HYPEREMIC AND SOFTENED DURING PREG AND MAY BLEED EPULIS OF PREGNANCY MAY DEVELOP BUT REGRESSES SPONTANEOUSLY HAEMORROIDS ARE COMMON CAUSED DUE TO CONSTIPATION AND ELEVATED PRESSURE IN V BELOW THE LEVEL OF ENLARGED UTERUS.

LIVER
HEPATIC BLOOD FLOW AND DIAMETER OF PORTAL VEIN INCREASES ALKALINE PHOSPHATASE ENZYME ACTIVITY IS INCREASED MOSTLY DUE TO PLACENTAL ALK PHOSPHATASE. AST, ALT, S. BILIRUBIN LEVEL IS SLIGHTLY LOWER S. ALBUMIN CONC. DECREASES 3.0 GM/DL(4.3), TOTAL ALBUMIN IS INCREASED, S GIOBULIN IS SLIGHTLY INCREASED. LEUCINE AMINOPEPTIDASE INCREASES WHICH CAUSES TRANSIENT DI

GALLBLADDER
CONTRACTION OF GALLBLADDER IS REDUCED WHICH LEADS TO INCREASED RESIDUAL VOLUME, IT IS DUE TO THE FACT THAT PROGESTERONE INHIBITS GALL BLADDER CONTRACTILITY. IMPAIRED EMPTYING LEADS TO STASIS WHICH IS ASSOCIATED WITH INCREASED BILE CHOLESTEROL SATURATION INCREASED PREVALANCE OF GALL STONES IN MULTIPAROUS . IHCP LINKED TO HIGH LEVEL OF CIRCULAING OESTROGEN WHICH INHIBITS INTRADUCTAL TRANSPORT OF BILE ACIDS.

CHANGES IN CARDIAC FUNCTION

 CHANGES IN CARDIAC FUNCTION BECOMES APPARENT DURING FIRST 8 WKS OF PREGNANCY. CARDIAC OUTPUT INCREASES AS EARLY AS 5TH WEEK OF PREGNANCY. BETWEEN 10 TO 12 WKS PLASMA VOLUME EXPANSION BEGINS, AND PRELOAD INCREASES.

HEART
AS THE DIAPHGRAM GETS ELEVATED HEART IS DISPLACED TO LEFT UPWARD AND IS ROATED ON ITS OWN AXIS (PALPITATION) APEX IS MOVED LATERALLY (4TH ICS,2.5CM OUTSIDE THE MID CLAVICULAR LINE) SOME DEGREE OF BENIGN PERICARDIAL EFFUSION IS PRESENT . LARGER CARDIAC SILHOUTTE ON CHEST RADIOGRAPH ON ECG THERE IS SLIGHT LEFT AXIS DEVIATION. CARDIAC SOUNDS:
EXAGGERATED SPLITTING OF FIRST HEART SOUNDS WITH LOUDNESS OF BOTH COMPONENTS NO CHANGE IN 2ND HEART SOUND A LOUD THIRD HEART SOUND SYSTOLIC MURMER IN 90 % OF WOMAN WHICH INTENSIFIED DURING INSPIRATION,DISSAPEARS SHORTELY AFTER DELIVERY(APICAL OR PULMONARY AREA WHICH IS DUE TO DEC BLOOD VISCOSITY( A SOFT DIASTOLIC MURMER IN 20 % CONTINOUS MURMER IN ARISING FROM BREAST VASCULATURE IN 10% MAMMARY MURMER

INCREASED VENTRICULAR MUSCLE MASS INDEX DOES NOT CORROSPONDS TO HYPERTROPHY

CARDIAC OUTPUT
CARDIAC OUTPUT AT REST INCREASES WHEN MEASURED IN LATERAL RECUMBENT POSITION
IT BEGINS TO INCREASE FROM 5TH WEEK OF PREGNANCY, REACHES ITS PEAK AT 30 TO 34WKS (40 TO 50%), INCREASES FURTHER DURING LABOUR (50%) AND IMMEDIATELY FOLLOWING DELIVERY(70%) OVER PRELABOUR VALUES.

MAP ALSO RISES. CARDIAC OUTPUT RETURNS TO PRE LABOUR VALUES BY 1 HOUR AND PREPREGNANT VALUES BY 4 WKS. INCREASED IN CARDIAC OUTPUT IS DUE TO
INCREASED IN BLOOD VOL MEET THE DEMAND OF INCREASED METABOLIC ACTIVITY

BLOOD PRESSURE
DECREASED DUE TO DECREASED SVR OVERALL DECREASE IN DIASTOLIC BP AND MEAN ARTERIAL BP IS BY 5 TO 10MM OF HG ARTERIAL PRESSURE USUALLY DEC TO A NADIR BY 24 TO 26 WKS AND RISES THERE AFTER FEMORAL VENOUS PRESSURE IS RAISED IT IS DUE TO PRESSURE EXERTED BY GRAVID UT ON THE COMMON ILLIAC VEINS MORE ON THE RT SIDE DUE TO DEXTROROTATION FEMORAL PRESSURE -- 8 TO 10CM WATER OF IN NONPREGNANT STATE; 25CM OF WATER IN LYING DOWN POSITION IN PREGNANCY AND 80 TO 100 CM OF WATER IN STANDING POSITION THIS EXPLAINS PHYSIOLOGICAL OEDEMA OF PREGNANCY SUBSIDES BY REST ALONE

DISTENSIBILITY AND STAGNATION OF VEINS EXPLAINS EDEMA,VARICOSE VEINS,PILES AND DVT

SUPINE HYPOTENSION SYNDROME

INCIDENCE-10% SUPINE COMPRESSION OF GREAT VESSELS BY UTERUS

URINARY SYSTEM

 GFR increaes by 25% by 2nd week of conception and 50% by the beginning of 2nd trimester. Due to this 60% of women report urinary frequency during pregnancy Animal studies have shown that relaxin and neuronal nitric oxide synthase ,responsible for increased GFR and RPF . Late in pregnancy urinary flow and sodium excretion average less than half the excretion rate in supine position compared with that in left lateral. Amino acids and water soluble vitamins are lost in greater amount Value of serum creatinine of 0.9mg/dl suggest underlying renal disease and should prompt further evaluation. During the day, pregnant woman tend to accumulate water as dependant edema and at night they mobilizes this fluid with diuresis; this causes nocturia and urine is dilute than in non pregnant state. Glucosuria increased GFR and impaired tubular reabsorptive capacity for filtered glucose. Protienuria is not evident; only evident during and soon after vigorous labour ; mean 24 hr excretion is 115mg/dl. Haematuria due to contamination during collection, difficult labour.

URETER
AS UTERUS ENLARGES IT ,IT RESTS UPON URETER LATERALLY DISPLACING AND COMPRESSING THEM AT THE PELVIC BRIM. UNEQUAL DILATATION OF URETER MORE ON RT SIDE (DEXTROROTATION ). RT OVARIAN COMPLEX RESTS LIES OBLIQUELY OVER RT URETER DURING PREGNANCY. URETER ELONGATION ACCOMPANIES DISTENSION ,WHICH IS IN TURN THROWN INTO CURVES OF VARYING SIZE. SMALL ONE IS SHARPELY ANGULATED. THEY ARE USUALLY SINGLE OR DOUBLE CURVE WHICH ON RADIOGRAPHS APPEAR AS ACUTE ANGULATIONS.

BLADDER
MOST CHANGES OCCUR AFTER 12 WKS. INCREASED UTERUS SIZE, HYPEREMIA OF ALL PELVIC ORGANS, HYPERPLASIS OF BLADDER MUSCLE AND CONNECTIVE TISSUE ELEVATES BLADDER TRIGONE AND CAUSES THICKENING OF ITS POSTERIOR AND INTRAUTERINE MARGIN ---- RESULTING IN MARKED DEEPENING AND WIDENING OF TRIGONE. BLADDER PRESSURE INCREASES FROM 8CM TO 20 CM OF WATER AT TERM TO COMPENSATE THE URETHERAL LENGTH (ABSOLUTE AND FUNCTIONAL) INCREASE URETHRAL PRESSURES BY 6.7 AND 4.8MM RESPECTIVELY, AT THE SAME TIME URETHRAL PRESSURE INCREASES BY 70 TO 93 CM OF WATER SO CONTINENCE IS MAINTAINED,STILL A THIRD OF WOMAN COMPLAIN OF INCONTINENCE OF URINE IN 3RD TRIMESTER (DD FOR RUPTURED MEMB) IN NULLIPARA PRESENTING PART ENGAGES BEFORE LABOUR SO BLADDER IS PUSHED UPWARDS AND FORWARDS CONVERTING ITS NORMAL CONVEX SURFACE INTO A CONCAVITY, PRESSURE FROM PRESENTING PART IMPAIRS BLOOD AND LYMPHATIC DRAINAGE SO BLADDER IS SUSEPTIBLE TO TRAUMA,INFECTION, AND BECOMES EDEMATOUS.

RESPIRATORY SYSTEM CHANGES

 Diaphragm rises by 4 cm during pregnancy THE TRANSVERSE DIAMETER OF THORACIC CAGE INCREASES BY 2CM AND SUBCOASTAL ANGLE WIDENS, THORACIC CIRCUMFERENCE INCREASES BY 6CM BUT IT IS NOT SUFFICENT ENOUGH TO PREVENT REDUCTION IN RESIDUAL VOLUME CREATED BY ELEVATED DIAPHGRAM PULMONARY FUNCTION CHANGES:

RESPIRATORY RATE IS UNCHANGED. TIDAL VOLUME AND RESTING MINUTE VENTILATION INCREASES SIGNIFICANTLY AS PREGNANCY ADVANCES. LOW EXPIRATORY RESERVE VOLUME AND COMPENSATED RESPIRATORY ALKALOSIS. ABOVE EFFECTS ARE DUE TO STIMULATORY EFFECT OF PROGESTERONE

 FRC AND RV DECREASED DUE TO ELEVATED DIAPHGRAM PEAK EXPIRATORY FLOW RATE DECLINES AS GESTATION ADVANCES LUNG COMPLIANCE UNAFFECTED AIRWAY CONDUCTANCE INCREASED AND TOTAL PULMONARY RESISTANCE REDUCED POSSIBLY AS A RESULT OF PROGESTERONE THE INCREASED OXYGEN REQUIREMENT AND CRITICAL CLOSING VOLUME MAKES RESPIRATORY DISEASES MORE SERIOUS DURING PREGNANCY. OXYGEN DELIVERY:
THE AMOUNT OF OXYGEN DELIVERED INTO LUNGS BY INCREASED TIDAL VOLUME EXCEEDS OXYGEN REQUIREMENT IMPOSED BY PREGNANCY. THE RTOTAL HB MASS AND IN TURN TOTAL OXYGEN CARRYING CAPACITY INCREASES APPRECIABLY . THUS, MATERNAL ARTERIO-VENOUS OXYGEN DIFFERENCE IS DECREASED

ACID BASE EQUILIBRIUM: PHYSIOLOGICAL DYSPONEA IS PRESENT DUE TO INCREASED TIDAL VOLUME WHICH LOWERS THE BLOOD PCO2. PROGESTERONE --- ACTS CENTRALLY AND LOWERS THE THRESHOLD AND INCREASES THE SENSTIVITY OF CHEMORECEPTORS RESPONSE TO CO2 TO COMPENSATE RESPIRATIORY ALKALOSIS -- PLASMA BICARBONATE LEVEL DECREASES BLOOD pH IS INCREASED ONLY MINIMALLY BUT SHIFTS THE HEMOGLOBIN DISSOCIATION CURVE TO LEFT . THE REDUCED PCO2 FROM MATERNAL HYPERVENTILATION AIDS CO2 TRANSFER FROM FETUS TO MOTHER AND RELEASES OXYGEN TO FETUS

THANK YOU