Essential hypertension can be defined as a rise in blood pressure of unknown cause that increases risk for cerebral, cardiac,

and renal events. In industrialised countries, the risk of becoming hypertensive (blood pressure >140/90 mm Hg) during a lifetime exceeds 90%. Essential hypertension usually clusters with other cardiovascular risk factors such as ageing, being overweight, insulin resistance, diabetes, and hyperlipidaemia. Subtle target-organ damage such as left-ventricular hypertrophy, microalbuminuria, and cognitive dysfunction takes place early in the course of hypertensive cardiovascular disease, although catastrophic events such as stroke, heart attack, renal failure, and dementia usually happen after long periods of uncontrolled hypertension only. All antihypertensive drugs lower blood pressure (by definition) and this decline is the best determinant of cardiovascular risk reduction. However, differences between drugs exist with respect to reduction of target-organ disease and prevention of major cardiovascular events. Most hypertensive patients need two or more drugs for blood-pressure control and concomitant statin treatment for risk factor reduction. Despite the availability of effective and safe antihypertensive drugs, hypertension and its concomitant risk factors remain uncontrolled in most patients.

Essential hypertension (also called primary hypertension or idiopathic hypertension) is the form of hypertension that by definition, has no identifiable cause. It is the most common type of hypertension, affecting 95% of hypertensive patients,
[1][2][3][4]

it tends to be familial and is likely to be

the consequence of an interaction between environmental and genetic factors. Prevalence of essential hypertension increases with age, and individuals with relatively high blood pressure at younger ages are at increased risk for the subsequent development of hypertension. Hypertension can increase the risk of cerebral, cardiac, and renal events.[5]

Contents [hide]

1 Classification 2 Risk factors 3 Pathophysiology 4 References [edit]Classification

The variation in pressure in the left ventricle (blue line) and the aorta (red line) over two cardiac cycles ("heart beats"), showing the definitions of systolic and diastolic pressure.

A recent classification recommends blood pressure criteria for defining normal blood pressure, prehypertension, hypertension (stages I and II), and isolated systolic hypertension, which is a common occurrence among the elderly. These readings are based on the average of seated blood pressure readings that were properly measured during 2 or more office visits. In individuals older than 50 years, hypertension is considered to be present when a person's blood pressure is consistently at least 140 mmHg systolic or 90 mmHg diastolic. Patients with blood pressures over 130/80 mmHg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment.[6]

Systolic pressure Classification mmHg

Diastolic pressure

kPa (kN/m2) mmHg kPa (kN/m2)

Normal

90119

1215.9

6079

8.010.5

Prehypertension 120139 16.118.5

8189

10.811.9

Stage 1

140159 18.721.2

9099

12.013.2

Stage 2

160

21.3

100

13.3

Isolated systolic hypertension

140

18.7

<90

<12.0

Source: American Heart Association (2003).

[6]

Resistant hypertension is defined as the failure to reduce blood pressure to the appropriate level after taking a three-drug regimen.[6]Guidelines for treating resistant hypertension have been published in the UK, and US.[7] [edit]Risk factors

Hypertension is one of the most common complex disorders. The etiology of hypertension differs widely amongst individuals within a large population.[8] And by definition, essential hypertension has no identifiable cause. However, several risk factors have been identified. Hypertension may be secondary to other diseases but over 95% of patients have essential hypertension which is of unknown origin. It is observed though that:

Having a personal family history of hypertension increases the likelihood that an individual develops HPT.

[9]

Essential hypertension is four times more common in black than white people, accelerates more rapidly and is often more severe with higher mortality in black patients.[9][10][11][12]

More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing. One of these genes is the angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number of AGT increases the blood pressure and hence this may cause hypertension.[8] Twins have been included in studies measuring ambulatory blood pressure; from these studies it has been suggested that essential hypertension contains a large genetic influence.[8] Supporting data has emerged from animal studies as well as clinical studies in human populations. The majority of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each has an elevated blood pressure as one of its phenotypic expressions. However, the genetic influence upon hypertension is not

fully understood at the moment. It is believed that linking hypertension-related phenotypes with specific variations of the genome may yield definitive evidence of heritability.
[13]

Another view is that hypertension can be caused by mutations in single genes, inherited on a Mendelian basis.

[14]

Hypertension can also be age related, and if this is the case, it is likely to be multifactorial. One possible mechanism involves a reduction in vascular compliance due to the stiffening of the arteries. This can build up due to isolated systolic hypertension with a widened pulse pressure. A decrease in glomerular filtration rate is related to aging and this results in decreasing efficiency of sodium excretion. The developing of certain diseases such as renal microvascular disease and capillary rarefaction may relate to this decrease in efficiency of sodium excretion. There is experimental evidence that suggests that renal microvascular disease is an important mechanism for inducing salt-sensitive hypertension.
[15]

Obesity can increase the risk of hypertension to fivefold as compared with normal weight, and up to two-thirds of hypertension cases can be attributed to excess weight.[16] More than 85% of cases occur in those with a Body mass index greater than 25.[16] A definitive link between obesity and hypertension has been found using animal and clinical studies; from these it has been realized that many mechanisms are potential causes of obesityinduced hypertension. These mechanisms include the activation of the sympathetic nervous system as well as the activation of the reninangiotensinaldosterone system.
[17]

Another risk factor is salt (sodium) sensitivity which is an environmental factor that has received the greatest attention. Approximately one third of the essential hypertensive population is responsive to sodium intake.[18] When sodium intake exceeds the capacity of the body to excrete it through the kidneys, vascular volume expands secondary to movement of fluids into the intra-vascular compartment. This causes the arterial pressure to rise as the cardiac output increases. Local autoregulatory mechanisms counteract this by increasing vascular resistance to maintain normotension in local vascular beds. As arterial pressure increases in response to high sodium chloride intake, urinary sodium excretion increases and the excretion of salt is maintained at expense of increased vascular pressures.[9] The increased sodium ion concentration stimulates ADH and thirst mechanisms, leading to increased reabsorption of water in the kidneys, concentrated urine, and thirst with higher intake of water. Also, the water movement between cells and the interstitium plays a minor role compared to this. The relationship between sodium intake and blood pressure is controversial. Reducing sodium intake does reduce blood pressure, but the magnitude of the effect is insufficient to recommend a general reduction in salt intake.[19] Renin elevation is another risk factor. Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked withaldosterone in a negative feedback loop. In consequence, some hypertensive patients have been defined as having low-renin and others as having essential hypertension. Low-renin hypertension is more common in African Americans than white Americans, and may explain why African Americans tend to respond better to diuretic therapy than drugs that interfere with the Renin-angiotensin system. High renin levels predispose to hypertension by causing sodium retention through the following mechanism: Increased renin Increased angiotensin II Increased vasoconstriction, thirst/ADH and aldosterone Increased sodium reabsorption in the kidneys (DCT and CD) Increased blood pressure. Hypertension can also be caused by Insulin resistance and/or hyperinsulinemia, which are components of syndrome X, or the metabolic syndrome. Insulin is a polypeptide hormone secreted by cells in the islets of Langerhans, which are contained throughout the pancreas. Its main purpose is to regulate the levels of glucose in the body antagonistically with glucagon through negative feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin. It has been suggested that vitamin D deficiency is associated with cardiovascular risk factors.
[20]

It has been observed that individuals with a vitamin D

deficiency have higher systolic and diastolic blood pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a "negative endocrine regulator of the renin-angiotensin system". Hence a deficiency in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed link between hypertension and vitamin D levels in the blood plasma.[21] Also, some authorities claim that potassium might both prevent and treat hypertension.[22] Recent studies claims that obesity is a risk factor for hypertension because of activation of the renin-angiotensin system (RAS) in adipose tissue,[23][24] and also linked renin-angiotensin system with insulin resistance, and claims that any one can cause the other.[25] Cigarette smoking, a known risk factor for other cardiovascular disease, may also be a risk factor for the development of hypertension.[26]

[edit]Pathophysiology

Main article: Pathophysiology of hypertension

A diagram explaining factors affecting arterial pressure

Cardiac output and peripheral resistance are the two determinants of arterial pressure. and soblood pressure is normally dependent on the balance between cardiac output and peripheral resistance.[27] Cardiac output is determined bystroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles. The pathophysiology of essential hypertension is an area of research, and until now remains not well understood, but many theories have been proposed to explain this. What is known is that cardiac output is raised early in the disease course, with total peripheral resistance (TPR) normal; over time cardiac output drops to normal levels but TPR is increased. Three theories have been proposed to explain this:

An overactive Renin-angiotensin system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension. An overactive sympathetic nervous system, leading to increased stress responses.

It is also known that hypertension is highly heritable and polygenic (caused by more than one gene) and a few candidate genes have been postulated in the etiology of this condition.[28][29][30]

INTRODUCTION When I began taking patient assessments from my four pregnancy case studies, I learned that one of the women (Client D) had experienced preeclampsia during her first pregnancy. As this condition may be a contraindication towards pregnancy massage, I asked her many questions about her experience before deciding whether or not I was able to consider her for pregnancy massage.

Based on the information provided during the Well Mother Pregnancy Massage course, additional information from further reading as well as from Client D, I also began to suspect that my other clients were showing signs of pre-eclampsia. I therefore became very interested in this particular condition because I wanted to ensure that I was treating each pregnant woman appropriately. Out of interest in their health and concern about their babies, it seemed an ideal opportunity to research the condition further and follow their progress as a project.

Until I began the research, I had little understanding or appreciation of the seriousness of this condition.

ECLAMPSIA and PRE-ECLAMSIA Pre-eclampsia is a condition that can affect expectant mothers usually in the last three months of pregnancy. This condition is the milder form of the condition eclampsia. Eclampsia is now less common due to more frequent ante-natal visits when pre-eclampsia can be diagnosed and treated early. Most maternity units will only manage 1 or 2 cases each year.

The cause is still not yet known or understood although a number of theories have been put forward to explain these two forms of the condition. Preeclampsia and eclampsia used to be called 'the toxaemias of pregnancy' which may suggest that it is a toxin that is responsible but this has not been proved.

When pre-eclampsia occurs, the blood flow to the pregnant woman's kidneys slows down. This will cause her to retain fluid. The blood flow from the mother to the placenta will then decrease and this reduces the amount of nutrients to the baby.

If pre-eclampsia becomes severe or continues for too long, the baby will not be able to grow properly. It is very important, therefore to make sure that the baby's development is monitored in the womb and regular measurements recorded. This is done by measuring fundal height, feeling the mother's abdomen and by ultrasound.

Pre-eclampsia and eclampsia can also occur after the actual birth of the baby, although this is extremely rare.

Statistics

Approximately 1 in 20 first pregnancies will result in pre-eclampsia.

Most women who suffer from pre-eclampsia in a first pregnancy deliver a normal healthy baby.

There is a higher risk of pre-eclampsia if the mother has any of the following conditions: multiple birth (expecting twins, triplets, etc.) first time pregnancy over the age of 35 diabetes renal failure

Eclampsia is rare, most maternity units will manage only one or two cases each year.

WHEN THINGS GO WRONG General

Very often a woman with pre-eclampsia is not even aware that anything is wrong: she may have gained excessive weight and her fingers and ankles may appear swollen. However, this is also a fairly common occurrence in any normal pregnancy.

Pre-eclampsia can be very mild and cause no problems. If however, it becomes worse and is not treated it can lead to eclampsia which is very serious for both the mother and baby. It can not only affect the growth of the baby but it can also cause convulsions which are life-threatening.

Regular antenatal appointments are crucial because a number of routine tests are conducted which may help to diagnose pre-eclampsia. Blood pressure is taken as well as a urine sample. It is important that these antenatal appointments are more frequent towards the end of a pregnancy when pre-eclampsia is more likely to develop.

Very high blood pressure and large amounts of protein in the urine indicate the threat of eclampsia. The mother may look extremely bloated due to fluid retention. She may also begin to experience headaches, blurred vision, or sensations of flashing lights (similar to migraine) as well as having pain just below the ribs. This can lead to feeling extremely ill and vomiting. It is imperative that the mother is treated urgently otherwise she could have fits, kidney failure and coma.

It has been said that pre-eclampsia is not easy to predict. If it is recognized early, it is possible to improve the symptoms by strict rest either at home or in a hospital.

It is a very delicate balance to try to keep both the mother and baby safe. The baby needs to stay in the womb long enough to mature and be able to survive after delivery. However, if the pre-eclampsia is left untreated for too long then it could be fatal for the mother. Careful monitoring of both mother and baby is therefore vital.

If the mother does have an eclamptic fit, her blood pressure will be lowered with drugs. Labour will then be induced and the baby delivered either normally or by emergency caesarean.

Usually the mother's blood pressure will return to a normal level after the birth of her baby. She will also pass large amounts of urine which will in turn reduce the swelling. There is a chance that the condition will recur in the next pregnancy, but it is usually less severe.

Signs and Symptoms of Pre-eclmsia

Sign / Symptom Cause Swelling of the arms, legs, face, hands Build up of fluid Severe headache / disturbed vision Hypertension Loss of appetite Uremia Nausea / vomiting Uremia Irritability / edginess / moodiness / memory loss / confusion / depression Uremia Tiredness / weakness / pale complexion Anemia Shortness of breath Anemia or fluid build-up Itching Increased phosphorus in the blood / dry skin Decreased urination Decreased amount of blood being filtered by the kidneys

Conditions and Complications (Pre-existing or Pregnancy Related)

Hypertension (High blood pressure) During pregnancy, blood pressure is checked at every antenatal appointment. A rise in blood pressure can be the first sign of pre-eclampsia, also known as Pregnancy Induced Hypertension (PIH), or Pre-Eclamptic Toxaemia (PET).

If blood pressure rises it increases the supply of blood for processing. This increased level of blood to the kidneys means an extra workload and more urine will be created.

Hypertension can increase the chance of stroke or heart attack.

Diabetes Long term or poorly managed diabetes can cause the blood vessels to decrease in size and therefore not allow enough blood to go through the kidneys.

Renal Failure The kidneys receive their instructions from the pituitary gland which produces Vasopressin which is an antidiuretic hormone. If there is a hormone imbalance it could cause the kidneys to produce too much urine and the body would become dehydrated.

Alcohol and caffeine do not affect the kidneys directly, however they slow down the pituitary's hormone production and the kidneys produce urine more rapidly. If these substances are taken in excess the body will become dehydrated.

Nicotine in cigarettes increases the production of the hormone. Heavy smoking will cause the person to urinate less frequently.

Diseases and Conditions of the Kidneys Hemolytic Uremia Syndrome (HUS) / Thromobocytopenia Purpuria (TTP) - are immune conditions. They have associated blood abnormalities such as anemia and low platelet counts. E Coli bacteria can be the cause of these conditions and although they are rare, they can cause kidney failure.

Nephritis - is the general term for inflammation of the kidneys often caused by infection by bacteria. There are two types of kidney inflammation.

'Pyelonephritis' and 'Glomerulonephritis' which is one of the leading causes of renal failure. Most infections can be controlled by antibiotics.

Polycystic - the kidneys develop cysts that enlarge and destroy normal tissue. This condition is genetic and inherited from parents.

Renal Cancer - one or both of the kidneys develops a cancerous growth. This can affect how they work and will need to be removed.

Nephron Damage - can also be caused by: Drugs and Poisons - anti-inflammatory drugs, such as paracetamol and aspirin may cause damage if large amounts are taken regularly.

Injury - from a kidney punch or car accident (for example).

Complications caused by Renal Failure Hypertension - can increase the chance of stroke or heart attack. Anaemia - causes tiredness and weakness. This is treated with medication and additional iron.

TESTING FOR PROBLEMS Urinalysis - a urine test will check for the presence of protein. Protein in the urine indicates that the kidneys filters are letting it escape from the blood. "Casts" - when the tubules are inflamed, solid matter (cells, fats, proteins) solidifies to the exact shape of the tubule. These casts are flushed out by urine.

Blood Test - to check if the blood contains too much urea. If it does it indicates that the kidneys are failing to get rid of the protein wastes.

CHANGES TO LIFESTYLE Diet

It would be beneficial to monitor and modify the diet if necessary because most of the wastes and extra fluids in the blood come from the food eaten. Eating a healthy diet during pregnancy and pre-conception will give the mother and baby optimum chance of preventing complications during pregnancy.

Kidney failure affects menstruation and therefore pregnancy is less likely to occur. If a woman wants to become pregnant, it is best in either the early stages of kidney failure or after a transplant. If a woman has conceived whilst suffering from kidney failure it is vital to control the intake of protein, potassium, sodium, phosphorus and fluids.

Minerals to control foods containing high amounts of the mineral Potassium - Potatoes, tomatoes, bananas, oranges, broccoli, chocolate and salt substitutions Phosphorus - Dairy products, nuts, colas, chocolate Sodium - Processed meats, bacon, crisps, pickles

* Consulting a qualified and experienced nutritionist who would work on an individual basis to balance all these nutrients would be highly recommended.

TREATMENT Conventional Treatment

The conventional treatment ranges from rest at home or in hospital drugs to lower the high blood pressure early delivery of the baby by induction or caesarean

Eclampsia (Greek, "shining forth"), an acute and life-threatening complication of pregnancy, is characterized by the appearance of tonic-clonic seizures, usually in a patient who had developedpre-eclampsia. (Preeclampsia and eclampsia are collectively called Hypertensive disorder of pregnancy and toxemia of pregnancy.) Eclampsia includes seizures and coma that happen during pregnancy but are not due to preexisting or organic brain disorders. [1]

[edit]Signs and symptoms

Typically patients show signs of pregnancy-induced hypertension and proteinuria prior to the onset of the hallmark of eclampsia, the eclamptic convulsion. Other cerebral signs may precede the convulsion such as nausea, vomiting, headaches, and cortical blindness. In addition, with the advancement of the pathophysiological process, other organ symptoms may be present including abdominal pain, liver failure, signs of the HELLP syndrome, pulmonary edema, and oliguria. The fetus may already have been compromised by intrauterine growth retardation, and with the toxemic changes during eclampsia may suffer fetal distress. Placental bleeding and placental abruption may occur. [edit]The eclamptic seizure Chesley distinguishes these four stages of an eclamptic event: In the stage of invasion facial twitching can be observed around the mouth. In the stage of contraction tonic contractions render the body rigid; this stage may last about 15 to 20 seconds. The next stage is the stage of convulsion when

involuntary and forceful muscular movements occur, the tongue may be bitten, foam appears at the mouth. The patient stops breathing and becomes cyanotic; this stage lasts about one minute. The final stage is a more or less prolonged coma. When the patient awakens, she is unlikely to remember the event.
[2]

In some rare cases there are no convulsions and the patient falls directly into a coma. Some patients may experience temporary

blindness upon waking from the coma . During a seizure, the fetus may experience bradycardia.[3] [edit]Risk factors

Eclampsia, like preeclampsia, tends to occur more commonly in first pregnancies and young mothers where it is thought that novel exposure to paternal antigens is involved. Further, women with preexisting vascular diseases (hypertension, diabetes, and nephropathy) or thrombophilic diseases such as the antiphospholipid syndrome are at higher risk to develop preeclampsia and eclampsia. Having a large placenta (multiple gestation, hydatiform mole) also predisposes women to toxemia. Further, there is a genetic component; patients whose mother or sister had the condition are at higher risk.[4] Patients who've experienced eclampsia are at increased risk for preeclampsia/eclampsia in a later pregnancy. [edit]Pathophysiology

While multiple theories have been proposed to explain preeclampsia and eclampsia, it occurs only in the presence of a placenta and is resolved by its removal.[5] Dr.Mayank suggested that placental hypoperfusion is a key feature of the process. It is accompanied by increased sensitivity of the maternal vasculature to pressor agents leading to vasospasm and hypoperfusion of multiple organs. Further, an activation of the coagulation cascade leads to microthrombi formation and aggravates the perfusion problem. Loss of plasma from the vascular tree with the resulting edema additionally compromises the situation. These events lead to signs and symptoms of toxemia including hypertension, renal, pulmonary, and hepatic dysfunction, and - in eclampsia specifically - cerebral dysfunction.[5] Preclinical markers of the disease process are signs of increased platelet and endothelial activation[5] Placental hypoperfusion is linked to abnormal modeling of the fetal-maternal interface that may be immunologically mediated[5] The invasion of the trophoblast appears to be incomplete.[6] Adrenomedullin, a potent vasodilator, is produced in diminished quantities by the placenta in preeclampsia (and thus eclampsia).[7] Other vasoactive agents are at play including prostacyclin, thromboxane A2, nitric oxide, andendothelins leading to vasoconstriction.[3] Many studies have suggested the importance of a woman's immunological tolerance to her baby's father, whose genes are present in the young fetus and its placenta and which may pose a challenge to her immune system.[8] Eclampsia is seen as a form of hypertensive encephalopathy in the context of those pathological events that lead to preeclampsia. It is thought that cerebral vascular resistance is reduced, leading to increased blood flow to the brain. In addition to abnormal function of theendothelium, this leads to cerebral edema.[9] Typically an eclamptic seizure will not lead to lasting brain damage; however, intracranial hemorrhage may occur. [10] [edit]Diagnosis

Seizures during pregnancy that are unrelated to preeclampsia need to be distinguished from eclampsia. Such disorders include seizure disorders as well as brain tumor, aneurysm of the brain, medication- or drug-related seizures. Usually the presence of the signs of severe preeclampsia that precede and accompany eclampsia facilitate the diagnosis.

Investigations CBC, RFT (Renal Function test), LFT (Liver Function test), coagulation profile, plasma rate concentration, 24 hour urine analysis, ultrasound [edit]Prevention

Detection and management of preeclampsia is critical to reduce the risk of eclampsia. Appropriate management of patients with preeclampsia generally involves the use of magnesium sulfate as an agent to prevent convulsions, and thus preventing eclampsia. [edit]Treatment

The treatment of eclampsia requires prompt intervention and aims to prevent further convulsions, control the elevated blood pressure and deliver the fetus. [edit]Prevention of convulsions Prevention of seizure convulsion is usually done using magnesium sulfate. from before 1955 when it was tested and publishedthe serum Mg considered: 4.0-7.0 mEq/L.
[12] 2+ [11]

The idea to use Mg

2+

for the management of eclamptogenictoxemia dates

therapeutic range for the prevention of the eclampsic uterine contractions is still
2+

As per Lu and Nightingale,

[13]

serum Mg

concentrations associated with maternal toxicity (also neonate depression or

hypotonia and low Apgar scores) are:

7.010.0 mEq/L - loss of patellar reflex 10.013.0 mEq/L - respiratory depression 15.025.0 mEq/L - altered atrioventricular conduction and (further) complete heart block >25.0 mEq/L - cardiac arrest

Even with therapeutic serum Mg2+ concentrations, recurrent convulsions and seizures may occurpatients would receive additional MgSO4but under close monitoring for respiratory, cardiac and neurological depression: 46 g loading dose in 100 mL IV fluid over 1520 min., then 2 g/hr as a continuous infusion.[3] If high Mg2+ concentrations fail to take effect, IV anticonvulsants will ease patient intubation and mechanical ventilation as adjuvants against the eclamptic convulsions (plus the hypermagnesemic thoracic muscle paralysis). Recently the long-term implications of the magnesium sulfate therapies were evaluated by the international MAGPIE study.[14] [edit]Antihypertensive management Antihypertensive management at this stage in pregnancy may consist of hydralazine (510 mg IV every 15-20 min until desired response is achieved) or labetalol (20 mg bolus iv followed by 40 mg if necessary in 10 minutes; then 80 mg every 10 up to maximum of 220 mg).[3] [edit]Delivery If the baby has not yet been delivered, steps need to be taken to stabilize the patient and deliver her speedily. This needs to be done even if the fetus is immature as the eclamptic condition is unsafe for fetus and mother. As eclampsia is a manifestation of a multiorgan failure, other organs (liver, kidney, clotting, lungs, and cardiovascular system) need to be assessed in preparation for a delivery, often a cesarean section, unless the patient is already in advanced labor. Regional anesthesia for cesarean section is contraindicated when a coagulopathy has developed. [edit]Invasive hemodynamic monitoring Invasive hemodynamic monitoring may be useful in eclamptic patients with severe cardiac disease, renal disease, refractory hypertension, pulmonary edema, and oliguria.[3]