Hypertension frequently accompanies stroke and often with high levels rise tensional This reagent has a protective effect on stroke immediately as an attempt to maintain adequate cerebral perfusion pressure to the area of ​​”ischemic penumbra” cerebral.

The decrease in mean arterial pressure by pharmacological levels below 100 to 110 mm. of Hg., aggressively, can cause severe neurological damage further.

Aortic Dissection

Aortic aneurysm is defined as a dilatation of the aortic diameter greater than 5 cms.
The most common cause is atherosclerotic and 40% of them are located in the ascending aorta, 35% in the descending thoracic aorta, 15% in the aortic arch and 10% in the thoracoabdominal aorta.

Other etiologies observed in thoracic aneurysms are autoimmune diseases, aortitis, collagen diseases, trauma and giant cell arteritis. The diagnosis should be suspected in front of chest pain trasfixiante, inequality or decreased pulses in the lower legs, abdominal pain, presence of aortic valve insufficiency.

Dysphagia, odynophagia, hemoptysis and superior vena cava syndrome are rare in the chest locations. About 50% of aortic aneurysms are asymptomatic and found incidentally. For these reasons must be ruled primarily in hypertensive crises.

Hypertension is frequently present in aortic dissection.
The drugs of choice for acute management are nitroprusside IV with the addition of a beta-blocker (Labetalol). The hydralazine is formally contraindicated.
The further management is determined by the place of suffering vascular, hemodynamic impact and availability of surgical treatment.

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It is the drug of choice in the management of hypertensive crisis associated with the exception of the pregnancy. It is a potent arterial vasodilator and intravenously administered venoso.Se pump infusion at a dose of 0.25 to 8 micrograms/kg/minute.

Its onset is rapid between 3-5 minutes and its effects (thiocyanates) occurs
by excessively rapid infusions or for prolonged periods of time. Thiocyanate toxicity causes blurred vision, tinnitus, confusion and seizures. Its excess can be removed by dialysis.

Nitroglycerin:

It is primarily a venous vasodilator. Its effect on the venous system is considerably greater than on the arterial system. It is administered by intravenous infusion pump at a dose of 5 to 100 micrograms/min. Its action begins between 2 and 5 minutes with a duration of 5 to 10 minutes. Among the side effects recorded headache and tachycardia. Like nitroprusside can cause cerebral vasodilation with increased intracranial pressure. Avoid use in patients with demonstrated hypersensitivity nitrites, severe anemia, shock, orthostatic hypotension, head trauma, closed-angle glaucoma, brain hemorrhage. Do not use in patients under medication with Viagra.

Diazoxide:

It is an arterial vasodilator with positive inotropic effect and concomitant increase in oxygen consumption. The dose used is 50-150 mgrs. Every 5 minutes or as an infusion at doses of 7.5 -30 mg / min. Diazoxide does not cross the blood brain barrier and has no effect on the cerebral circulation but this is part of the eventual fall of systemic pressure below the cerebral perfusion pressure. Its action begins between 1 and 5 minutes and lasts between 4 and 24 hrs. Severe side effect may refer the interruption of delivery and pancreatic toxic effect of hyperglycemia.

Labetalol:

Beta and alpha blocker combination. Dose: 2 mg / min. IV or 20 mgrs. initial followed by 80 mgrs. every 10 minutes with a maximum dose of 300 mgrs.Su action begins in less than 5 minutes and lasts between 3 and 6 hrs.Es highly effective antihypertensive treatment can be continued orally. It has a formal indication in the pharmacological management of aortic dissection. And can be used in almost all hypertensive crisis, except in the presence of heart failure beta effect.

Hydralazine:

Arterial vasodilator. 10-20 mgrs IV dose onset of action in 10-30 minutes and lasts for 2 to 4 hrs. The hydralazine can cause myocardial infarction or angina pecho.Formalmente contraindicated in the treatment of aortic dissection.

Propranolol:

Beta blocker. EV has indicated (1-10 mgrs loading dose followed by 3 mgrs/hour).
Its action begins at 2 pm. and its use is restricted to be complementary to a vasodilator in order to prevent tachycardia as blood pressure does not drop sharply.

Enalaprilat:

Inhibitor of converting enzyme. Dose: 1.25 to 5 mgrs IV every 6 hrs. The action begin in 15 minutes and lasts between 12 and 24 hrs. The enalaprilat may have a variable response often excessive, although its effects on cerebral autoregulation prevents the reduction of cerebral blood flow by decreasing the pressure systemic. Present absolute contraindication for use during pregnancy.

Nifedipine:

Calcium channel blocker. Sublingual or oral dosing 10-20 mgrs.Comienzo of action between 5 and 15 minutes that lasts between 3 and 5 hrs. Presents a response variable and unpredictable too often so it should be administered with extreme caution in elderly or in patients with stroke.

Esmolol:

Cardioselective beta blocker with a fast metabolism so its half-life of 10 minutes and lasts for 30 minutes. It is used successfully in hypertensive crisis occurs or post-extubation intraanestesia.

Phentolamine:

Alpha agonist. It is administered IV at a dose of 5 mgrs. Its use is restricted to hypertensive crisis caused by pheochromocytoma. Among its side effects include: tachycardia, cardiac arrhythmias and ischemic events.

Nimodipine:

Calcium channel blocker. When EV is administered there is decreased blood pressure with little effect on heart rate and small increases in cardiac output. Its use is currently restricted to use in subarachnoid hemorrhage as an adjunct in reducing vasospasm.

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- Establish an intravenous
- Establish, if available, an arterial line to monitor blood pressure
- Place a heart monitor
- Make two questions:
How quickly should I lower blood pressure?
To what level should I lower it?

To answer these questions must base its criteria on the following premises:

Age: critical care in elderly patients to prevent ischemic cerebrovascular events with aggressive antihypertensive therapy

Depletion of volume: the diuresis induced by hypertension patients deplete the volume and orthostatic hypotension.

Consider the previous antihypertensive medication and duration of hypertension.
Prolonged hypertensive disease produces anatomical and functional changes in arteries that magnify the effects of acute antihypertensive therapies.

Consider the existence of concomitant diseases, mainly of renal

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Central Nervous System is impaired when the blood pressure levels beyond the capacity of cerebral autoregulation to maintain a perfusion pressure constante.Con pressure increases there is a reaction that vasoconstriction is exceeded when the pressure levels reach a certain level . There is then a transudation through the capillaries, with progressive anatomical damage to the arteriole and fibrinoid necrosis.

These changes lead to progressive loss of autoregulation and cardiovascular system parenquimatoso.El ischemic damage is affected by a disproportionate increase in afterload which can lead to myocardial failure with pulmonary edema, myocardial ischemia and myocardial infarction.

The kidney function decreases when chronic hypertension accelerates atherosclerosis fibrinoid necrosis with an overall decrease and gradual self-systems of renal blood flow.
The approach to the patient in hypertensive crisis is a systematic evaluation

History:

* Distinguish between hypertensive emergency (with organ damage present) of the urgenciaHipertensiva (no organic damage present.)
* Is the Pre Hypertension?
* What is the duration?
* Is there prior renal disease?
* Is there a history of:
- Peripheral edema
- Orthopnea
- Dyspnea on exertion
- Symptoms and / or neurological deficit
- Hematuria, oliguria
* Was patient Premedication?
* Current Medication
* Use or abuse of illicit drugs:
-Amphetamine
-Cocaine
-LSD
CNS-Stimulants
- Abandonment recent antihypertensive medication especially
Clonidine and Beta Blockers

Physical examination

* Record the blood pressure sitting and standing
* Record the pressure in upper and lower extremities to assess differences in tension and evaluating aortic disease.
* Eye Fund, helps to distinguish between hypertensive emergency (normal fundus without bleeding and exudates), Hypertensive Emergency, frequently associated with papilledema and hard exudates.
* Exam Cardiovascular
-Presence of aortic insufficiency
-Gallop by R3 or R4
Presence of abdominal pulsatile mass
-E.C.G.: Define ischemia, infarction in progress
-LVH and arrhythmia

Neurological examination

Mental state and focal signs.

Laboratory

- Urinalysis to rule out hematuria and proteinuria
- Peripheral smear: discard hemolysis (Esquiztocitos)
- Urea and Creatinine: Assess renal failure
- Ionograms
- Pregnancy test Possible

Imagery

- CXR: lung edema rule
- Ensachamiento mediastinal (aortic aneurysm)
- T.A.C. Brain: exclude cerebral edema, hemorrhage, myocardial

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Hypertensive emergency is characterized by symptoms of severe hypertension (conventionally, but not limited) to a diastolic pressure of 110 mm. Hg.con involvement of an organic system (CNS, cardiovascular or renal disease) from which the pressure should be lowered within a period of minutes or hours.

Hypertensive emergencies associated with hypertensive encephalopathy, intracranial hemorrhage, stroke and acute pulmonary edema, myocardial infarction, adrenergic crisis, dissecting aortic aneurysm, and eclampsia. Hypertensive emergencies occur more often in men than in women and a higher incidence between 40 and 50.

Hypertensive urgency is a potential risk, which has not caused damage to target organs and allows the pressure can be decreased progressively within a period of 48-72 hrs.

Hypertensive emergencies are associated with the following entities:

- Malignant hypertension
- Unstable Angina
- Postoperative Hypertension
- Preeclampsia.

The most common causes of sudden rise in blood pressure in a patient with chronic essential hypertension are:

- Renovascular Hypertension
- Eclampsia
- Pre-eclampsia
- Acute glomerulonephritis
- Pheochromocytoma
- Abandonment of antihypertensive medication
- Head trauma and Central Nervous System
- Renin-secreting tumors
- Drug-induced hypertension
- Burns
- Vasculitis
- Idiopathic thrombocytopenic purpura
- Postoperative Hypertension
- Coarctation of the aorta

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In these patients is more useful measure ambulatory blood pressure (MAP) as often lose the nocturnal blood pressure and this is evidenced by the record during sleep. This lack of decline is also a predictor of renal damage and mortality.

Hypertension in patients with renal disease is more sensitive to changes in plasma volume directly related to salt intake. The maintenance diets low in sodium (1 to 2 g daily) helps provide a good control of blood pressure and facilitates the action of drugs. However, a very intense sodium depletion can lead to hypovolemia.

The therapeutic goal is stricter than in other patients because the patient more susceptible to renal vascular damage. The figures should be kept below 130/80 mmHg in moderate kidney disease and below 125/75 mmHg when renal involvement is advanced.

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There are two forms of kidney involvement. The acute in hours or days that function is lost and in many cases you can return to recover, and chronic condition in which the damage occurs over years.

Often there are no symptoms until it has lost a high percentage of renal function. Sometimes the only symptom of kidney damage is the presence of hypertension.

How do I know if I have kidney failure?

Because it is asymptomatic until very advanced stages of knowing how the situation of renal function is to conduct analytical parameters which determine the level of urea and creatinine, sodium and potassium in the blood, the acidity of the blood and urine excretion of these elements and proteins.

For each person is calculated glomerular filtration rate from a complex mathematical formula involving the age, race, weight and height values ​​as well as substances found in blood and urine.

What does having microalbuminuria?

The loss of protein in the urine is called proteinuria. When proteins that are lost are small in size as albumin speak of albuminuria and if the range of loss is small, microalbuminuria.

Proteinuria greater the greater the progression of renal damage. First, this parameter was associated with diabetes in which microalbuminuria is established as an early marker of kidney damage. Later it was found that the presence of microalbuminuria in other kidney diseases, no diabetes, and even healthy people can also be a single factor and vascular risk predictor of mortality similar to hypercholesterolemia or personal history of heart disease.

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The kidney is the organ responsible for filtering the blood, purging toxic substances, is also producing substances that help regulate the production of red blood cells, erythropoietin, and involved in maintaining blood pressure, renin .

The kidney is involved in the pathways regulating blood pressure and maintaining blood volume, is involved in the development of hypertension when one of its many functions are not executed properly and is the target organ of hypertension, as it is one who suffers more damage when blood pressure levels is permanently high.

What is kidney failure?

It is the result of failure in kidney function, blood stops purged so that poisons accumulate, some of them such as urea, resulting from the degradation of proteins, which when found in high amounts can cause coma.

It is manufactured erythropoietin, and this alters the production of red blood cells and leads to anemia.

Regulatory mechanisms are impaired blood pressure and hypertension appears.

Substances in urine are lost that should be recovered or not filtered as albumin.

It alters the balance of lipids in the body and increase cholesterol levels, cardiovascular risk factors adding and promoting the development of atherosclerosis.

Finally do not regulate certain ions in the blood such as potassium, whose presence in very high quantities can cause arrhythmias and death.

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This name is given to an increase in steroid production (cortisol) in the body by the existence of a tumor in the pituitary or adrenal glands, but can also be caused by taking steroids chronically (much more common for earlier).

The higher level of steroids can cause hypertension, diabetes or glucose intolerance, obesity, which is distributed in a particular way on the trunk and neck, skin striae vinous color, moon face, muscle weakness, fatigue and osteoporosis and others.

Characteristics of hypertension in Cushing

Hypertension affects more than 80% of patients with Cushing’s syndrome and is often difficult to treat serious. It is thought that gravity can be related to the loss of nocturnal dip in blood pressure.

The mechanisms causing hypertension in these patients is sodium retention produced by steroids.

Blood pressure tends to normalize just months after surgical correction of producing tumor (when they were the cause) but often persist atherosclerotic risk factors for abdominal obesity and insulin resistance.

Medical treatment of this type of hypertension is the same as essential hypertension, although it benefits more from the use of diuretics antialdosterone effect.

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- Personal Hygiene: Wash your feet often drying properly before putting on socks and shoes. Areas dry thoroughly between the toes.

- Take precautionary measures in public places like swimming pools, gyms, showers, etc..

- Use of appropriate footwear that allows the foot sweat.

- Use cotton socks or wool. Change them often and whenever they are wet.

What is the treatment?

There are basically two types of treatment (often used in combination):

Topical treatments (applied directly to the nail)

Coatings are applied on the surface of the nail. They require hard work, diligence and awareness as they are often long term treatment and its application requires a time (nail filing, product application). Usually sufficient to treat skin infections and when the involvement of the nail is not very long (should not affect the root of the nail).

Some of the drugs used topically include amorolfine, and tioconazole ciclopiroxolamine.

Systemic treatments (administered orally)

Its efficiency is higher. The duration of treatment is also usually long (several months).

Some of the drugs used are oral terbinafine and itraconazole.

When these treatments are not effective, you can get to make the total nail removal (ablation) by surgical or chemical methods.

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