Hypertension in Pregnancy

Hypertension in Pregnancy

Normal Changes in Blood Pressure

·        Physiology:

o   ­O2 consumption from 300 to 350 ml per minute 

o   ­CO from 5 to 6.5 - 7 litres per minute due to ­Stroke volume (10%) and ­HR (15 bpm)

o   Peripheral resistance falls (due to hormonal changes)

o   ¯PCO2 to 31 mm Hg to increase gradient for shifting CO2 from fetus 

o   ­Blood volume by 40% from early pregnancy to delivery

o   ­Ventilation

o   ­Glomerular filtration ® ­urination 

·        During first and second trimesters, BP (especially diastolic) falls by 10 - 20 mmHg, return to booking BP by 3^rd trimester (partly due to hypotension ® ­aldosterone)

·        Venous distensibility + ­venous pressure predispose to varicose veins

Essential Hypertension

·        Present before pregnancy and commoner in older multips

·        If high blood pressure before 20 weeks, probably pre-existing hypertension

·        Aim to keep BP < 140/90

·        5 * more likely to develop pre-eclampsia than normotensive women

·        Watch for „white-coat‟ hypertension

Pre-eclampsia

·        = Pregnancy-induced hypertension with proteinuria +/- oedema

·        = Toxaemia

·        = Pre-eclampsic toxaemia (PET)

·        = Gestational Hypertension

·        Signs: > 20 weeks pregnant, oedema, proteinuria, ­BP (­systolic by 20 - 25 or ­diastolic by 15 over booking BP) 

·        If < 20 weeks then ?hydatiform mole 

·        Is asymptomatic Þ requires screening

·        May recur in a subsequent pregnancy

·        Risk factors:

o  Primiparity

o  New partner

o  Previous or family history of pre-eclampsia or eclampsia

o  Overweight

o  < 20 years or > 35 years 

o  Multiple pregnancy (or anything else that ­placenta size)

o  Renal disease, essential hypertension, diabetes

o  IVF

o  Autoimmune disease (eg SLE, anti-phospholipid syndrome)

·        Presentations:

o  In „normal‟ pregnancy (ie low risk) – PET is usually mild and late (eg from 37 weeks)

o  In „abnormal‟ pregnancy, may begin from as early as 20 weeks and be severe 

·        Pathogenesis: Abnormal vascularisation of the placental decidua by the syncytiotrophoblast during the secondary invasion (~ 28 weeks). Arterial wall in placenta does not distend enough to allow sufficient blood flow to placenta in late pregnancy ® Mother doesn‟t get the right pregnancy triggers from the placenta ® mother‟s body doesn‟t completely adapt to being pregnant

·        Effects:

o  Mother doesn‟t vasodilate sufficiently ® ­BP, ¯plasma volume and ­peripheral resistance

o  Generalised oedema eg face

o  Proteinuria is a late sign Þ renal involvement.  Oliguria Þ renal failure

o  Serious signs (® Urgent admission): 

§  Signs of ­ICP: headaches, vomiting, hyperreflexia, bilateral clonus

§  Headache, stomach pain, vomiting, ­HR (ie mimics viral illness) 

§  Sustained vasoconstriction ® ischaemia (eg visual changes, brain) and ­clotting/DIC. Also effects liver (RUQ pain), kidneys 

§  Placental abruption

§  Placental ischaemia

·        Effects on fetus:

o  Asymmetric growth retardation (brain preferentially preserved) 

o  If untreated ® symmetric growth retardation (if this occurs on its own then pre-existing fetal abnormality) 

o  ¯Fetal movements, fetal respiratory effort and ¯amniotic fluid

·        Assessment:

o  Baby: CTG and US

o  Mum:

§  Most important of the following are platelets and uric acid

§  FBC: 

·        Either ­Hb (haemoconcentration secondary to oedema) or ¯Hb (haemolysis secondary to DIC) 

·        ¯Platelets – adhering to damaged capillary endothelium 

§  Liver function tests: ­AST/ALT (not ALP – that‟s produced by the placenta). NB exclude acute fatty liver of pregnancy 

§  Creatinine and Uric Acid: ­ due to ¯renal flow. If bad then 24 hour urine to check for oliguria/renal failure 

§  Coagulation: ¯fibrinogen due to DIC

·        Treatment: 

o  Low dose aspirin ® pregnancy runs closer to term (controversial)

o  Mild: monitor BP and fetus; rest up (but not bed rest).  If problems and > 37/40 then induce

o  Moderate: (eg BP of 140/90 but stable): 

§  Labetalol (want b2 activity without any a activity).  Contraindicated in asthma

§  Methyldopa (causes depression etc but safe for the fetus)

§  Nifedipine (other Ca blockers cause fetal malformations)

·        : Hydralazine IV (¯BP). Aspirin (blocks thromboxane production ® preferentially make prostacyclin), antihypertensives, anticonvulsant prophylaxis (Magnesium sulphate). Have to stabilise before delivery 

·        Delivery is the only cure (although > half of fits occur post partum). Antihypertensives only mask the disease. Diuretics contra-indicated. May have serious illness with only mild proteinuria (1+). Usually resolves over 10 days. 

·        Deliver now if ¯platelets, signs of renal failure, unstable BP etc (ie signs of serious disease), or if at term (>37 weeks)

Eclampsia

·        1 in 2000 pregnancies

·        Major cause of maternal and fetal morbidity/mortality

·        Is unpredictable.  BP is not a good marker of disease

·        Generalised seizures (eclampsia) – treat with Magnesium sulphate (better than diazepam)

·        Death from stroke (most common), liver, kidney or heart failure