Volume-5 | Issue-52 | March 5, 2014

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Healthy HeartHonorary Editor :

Dr. Hemang Baxi

From the desk of Hon. Editor:

Warm Greetings & Happy Holi

to everyone

High Blood Pressure complicates

approximately 6-8 % of all

pregnancies and remains a

major cause of morbidity &

mortality for mother and foetus.

A relative paucity of

investigative data as well as the

frequent difficulty in making an

etiological diagnosis on clinical

criteria alone may be among

the reasons why there are many

conflicts about the

management of hypertension

during pregnancy. In this issue,

I have tried to summarise

current concepts regarding

hypertensive disorders of

gestation.

- Dr. Hemang Baxi

Hypertension in Pregnancy

Case History

Mrs. X is 32 years old and 29 weeks into

her first pregnancy. To date, the

pregnancy has been uncomplicated and

recent ultrasound scans confirmed

normal foetal size for estimated gestation,

and that there were no foeta l

abnormalities. She attends for routine

review and her blood pressure (BP) is

150/95. Her BP was also high the previous

week. Her pre-pregnancy health was

excellent, and there is no history of

hy p e r t e n s i o n . H e r m o t h e r h a s

hypertension. Urine analysis is negative

for protein.

u How should this be investigated

further?

u What is the threshold for starting

antihypertensive treatment?

u What is the target BP for this patient?

u Which agents are safe and effective in

pregnancy?

Background

Hypertensive complications are present in

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6-8% of pregnancies, representing the

commonest medical d isorder in

pregnancy. BP should be measured with

the patient rested and sitting with the arm

horizontal and supported. Diastolic BP

(DBP) is defined as disappearance of the

Korotkoff V sound. High values should be

repeated on a separate occasion.

Hypertension is defined as:

u Mild: systolic BP (SBP) 140-159 mmHg,

DBP 90-109 mmHg

u Severe: SBP ≥160 mmHg, DBP ≥110

mmHg

Gestational hypertension occurs after 20

weeks and usually resolves before 12

weeks postpartum. By definition, there

are no vascular complications of

established hypertension nor are there

signs or symptoms of pre-eclampsia.

There is an increased risk of pre-eclampsia

– the earlier hypertension develops, the

greater the risk.

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Volume-5 | Issue-52 | March 5, 2014

Chronic hypertension occurs when there

is pre-pregnancy hypertension, or

sustained increase in BP prior to 20

weeks of gestation. It complicates 3-5%

of pregnancies.

Mild pre-eclampsia when the following

criteria apply:

u SBP >140 mmHg and/or DBP >90

mmHg or SBP 20 mmHg greater than

pre-pregnancy or early pregnancy

value and/or DBP increased by >10

mmHg above pre-pregnancy or early

pregnancy

u >20 weeks of gestation

u Proteinuria – albumin/creatinine

ratio >25 mg/mmol on spot testing or

>300 mg/24 h on timed collection

u A b s e n c e o f n e u r o l o g i c a l

complications

Severe pre-eclampsia – when the above

criteria are fulfilled but:

u SBP >170 mmHg and/or DBP is >110

mmHg

but consider with lesser degrees of

hypertension when there is:

u severe proteinuria (>5000 mg per 24

h);

u oliguria (<400 ml/24 h);

u thrombocytopenia (<100 000/ml);

u elevated liver enzymes (>3 X normal);

u neurological symptoms (headache,

b l u r r e d v i s i o n , i m p a i r e d

consciousness);

u pulmonary oedema; and

u intrauterine growth restriction

(IUGR).

Eclampsia – the patient fulfills the

c r i ter ia for pre -ec lamps ia and

convulsions (in the absence of pre-

existing epilepsy or predisposition to

epilepsy).

HELLP (Haemolytic anaemia, Elavated

Liver enzymes and Low Platelets) is a

form of severe pre-eclampsia where

there is a high risk of maternal mortality.

Gestational hypertension implies a

temporar y d i sorder re lated to

pregnancy. This diagnosis is often only

clear in retrospect when BP returns to

normal following delivery. It is an

important diagnosis as 20-40% of

patients develop pre-eclampsia. The

latter is more likely when hypertension is

severe, there has been previous

pregnancy hypertension, a history of

miscarriage, or where hypertension

develops early. When hypertension

develops late in pregnancy, the proven

benefits of treatment are mainly to the

mother rather than the foetus. When

diagnosed very late in pregnancy it is not

clear that aggressive treatment of

hy p e r te n s i o n rat h e r ex p e c ta nt

treatment with careful timing of delivery

is warranted.

Incidence and severity of chronic

hypertension varies between racial

groups, and is particularly high in African

Americans. For women mild to moderate

hypertension and no end-organ damage,

the risk during pregnancy is low and they

often do not need change to their pre-

pregnancy treatment. There is, in any

case, a physiological lowering of BP

during pregnancy. Risks to the mother

include pre-eclampsia, abruption

placentae, renal impairment, stroke and

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Healthy HeartVolume-5 | Issue-52 | March 5, 2014

pulmonary oedema. Of these pre-

eclampsia is by far the commonest (50-

7 5 % o f w o m e n w i t h s e v e r e

hypertension). There is no evidence that

any specific therapeutic agent or

achievement of ant specific BP target

prevents pre-eclampsia. Risks to the

foetus are miscarriage (with early

pregnancy hypertension), prematurity

and intrauterine growth retardation

(IUGR). The presence of hypertension

greatly increases the cost of pregnancy

with increased clinic visits and tests,

medications, greater likelihood of

hospital admission and operative

delivery.

Thresholds for treating hypertension and

treatment targets vary between

guidelines. It is reasonable to initiate

treatment when SBP is >150 mmHg and

when DBP is >95 mmHg. A target of

130/85 seems reasonable and can

f requent ly be ach ieved. These

thresholds may need to be varied

according to the perceived risk of the

patient. SBP is often relatively more

increased in pregnancy than is DBP.

Monitoring is required to detect foetal

distress related to decreased placental

perfusion, and its presence will affect

timing and mode of delivery. Drug

treatment is generally based on long

experience with drugs known to be safe,

rather than on extensive trials.

Methyldopa and labetalol are still

considered the first-line agents, followed

by n i fed ip ine and hydra laz ine.

Ang iotens in -convert ing enzyme

inhibitors and angiotensin receptor

blockers are contraindicated in

pregnancy (Box 1).

All women with hypertension in

pregnancy should have measurement of

proteinuria, defined as protein excretion

≥ 300 mg per day in a timed 24-h

collection, or ≥30 mg/mmol creatinine

in a spot collection. Plasma creatinine

and electrolytes should also be

measured. ECG and fundoscopy will

exclude end-organ damage in patients

with chronic hypertension. A routine

chest X-ray is not justified.

Treatment Options:

M e t h y l d o p a i s c o n v e r t e d t o

α–methylnoradrenaline, which acts as a

central α -adrenergic agonist. There is no 2

evidence of teratogenicity of cognitive

defects in children exposed to this agent

in utero. It may cause fatigue,

depression, sleep disturbances and dry

mouth. A minority (5%) have increased

liver enzymes. Long-term use can cause

more serious hepatic side effects,

antinuclear factor positivity and

Coombs' positive haemolytic anaemia.

Usual daily dose is 500-3000 mg in two to

four doses.

Box 1

Ang iotens in -convert ing enzyme

inhibitors and angiotensin receptor

blockers are contraindicated in

pregnancy because of risk of cardiac and

renal defects, oligo-hydramnios and

IUGR.

Labetalol and other β-blockers This class

of drugs has been widely used in

pregnancy, and is not thought to be

teratogenic. There is risk of IUGR,

perhaps because of decreased placental

blood flow. β-blockers are almost

c e r t a i n l y m o r e e f fe c t i v e t h a n

methyldopa at lowering BP. Atenolol is

probably best avoided because of risk of

decreased placental function leading to

decreased placental weight and IUGR, as

well as the risk of foetal bradycardia and

neonatal hypoglycaemia. Labetalol

combines peripheral β-blocking activity

with α -blocking activity. It is effective 1

and safe, though not completely devoid

of potential to cause IUGR and neonatal

hypoglycaemia. Side effects include

fatigue, mood and sleep disturbance,

and bronchoconstriction. A usual daily

dose is 200-1200 mg in two to three

doses.

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Calcium channel blockers Nifedipine is

the most widely used of these drugs in

pregnancy. Nicardipine, felodipine and

verapamil have also been used.

Neuromuscular blockade leading to

profound weakness and myocardial

depression have been reported when

used with magnesium as a prophylactic

treatment for eclamptic fits. Common

side effects are flushing, headache,

tachycardia and peripheral oedema.

Long-acting preparations are preferred

with a total daily of 30-120 mg.

Hydralazine acts as a direct vasodilator

and has been used widely, both in the

management of chronic hypertension in

pregnancy and in the acute management

of severe hypertension. Side effects

include headache, nausea, flushing and

palpitations. Long-term use can lead to

peripheral neuropathy or drug-induced

lupus. A usual daily dose is 50-300 mg in

two to four divided doses.

Diuretics, e.g. hydrochlorthiazide 12.5 or

25 mg daily is thought to be safe. It may

decrease the fluid retention experienced

with vasodilator drugs.

When BP is >160/110, particularly with

encephalopathy, end-organ damage

(cardiac or renal failure) or eclampsia, BP

should be reduced urgently by 25%, and

thereafter more gradually to less than

160/100. Management should be

undertaken in hospital with careful

maternal and foetal monitoring. The

commonly used agents are:

1. Labetalol, 10-20 mg IV followed by

20-80 mg infusions every 30 min to a

maximum of 200 mg.

2. Hydralazine, 5 mg IV followed by 5-10

mg every 30 min.

3. Nifedipine, 10-30 mg orally or

sublingually (short-acting capsules).

Patients should continue to be

monitored and, where necessary,

receive treatment following delivery. For

patients with gestational hypertension

or pre-eclampsia, hypertension is usually

improved within days but may take up to

a few weeks. Similarly, chronic

hypertension often improves within

weeks of delivery. Women should be

encouraged to breast-feed where

possible. Many drugs are safe and not

concentrated in breast milk (Box 2).

Atenolol and metoprolol should be

avoided.

BOX 2 Antihypertensive drugs safe

during breast-feeding

1. Angiotensin-converting enzyme

inhibitors: captopril, enalapril

2. β–blockers: labetalol, propranolol,

nadolol, oxprenolol and timolol

3. Vasodilators: hydralazine and

minoxidil

4. Calcium channel blockers: diltiazem,

verapamil and nifedipine

5. Centrally-acting: methyldopa

6. Other: spironolactone

Congratulations to

Dr. Vineet Sankhla

for receiving FISE

(Fellowship of Indian

Society of

Electrocardiology)

Congratulations to

Dr. Ajay Naikfor being elected as the

President of the

Indian Society of

Electrocardiology for the year

2014-2015

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