Kills Slowly

Kills Slowly

Hypertension a disease that kills

Hypertension is a disease of diverse causes. And which is manifested by the sustained increase in blood pressure, or in systole and diastole in both.

The increase in blood pressure (hypertension) is a major cause, but more susceptible to treatment, disease, and is divided into primary and secondary schools. In the general population, blood pressure is a continuous variable and its increase is associated with an increased risk of disease. Hypertension can be arbitrarily defined as a sustained diastolic pressure greater than 90 mmHg. However, there is no risk of a disease in which blood pressure is a pathogenic factor.

Primary hypertension (essential) is the elevation of blood pressure with age, but without apparent cause. Represents over 90% of cases and usually appears after age 40 The phenotype of high blood pressure in hypertension is due to an interaction between genetic predisposition, obesity, alcohol consumption, physical activity and other factors not yet identified .

Secondary hypertension, which represents about 10% of cases, is due to an identifiable cause, the most frequent renovascular disease, which raises blood pressure by activating the renin-angiotensin-aldosterone. Depending on their clinical course, both the primary and secondary hypertension can be classified into two types. In benign hypertension, there is a stable elevation of blood pressure for many years, whereas hypertension accelerated the elevation of blood pressure is intense and worsens in a short time.

Factors that regulate blood pressure

Blood pressure can be raised by increasing the volume of cardiac or peripheral vascular resistance. The first rises with increasing blood volume or contractility and heart rate, the second can be enhanced by humoral factors, neural and self.

According to the degree of damage produced organic, hypertension can be found in different stages:

PHASE I: No functional changes.

PHASE II: The patient shows one of the following signs, even when you are asymptomatic.

a) left ventricular hypertrophy (palpation, chest radiograph, ECG, echocardiogram).
b) Angiotonía in retinal arteries.
c) Proteinuria and / or slight elevation of creatinine (up to 2 mg / d).
d) arterial atheroma plaque (radiography, ultrasonography) in carotid arteries, aorta, iliac and femoral.

PHASE III: symptomatic manifestations of organic injury:

a) Angina pectoris, myocardial infarction or heart failure.
b) transient cerebral ischemia, cerebral thrombosis and hypertensive encephalopathy.
c) Exudates and retinal hemorrhages, papilledema.
d) Chronic renal insufficiency.
e) aortic aneurysm or atherosclerosis obliterans of lower limbs.

The thickening of the arterial wall and arteriolosclerosis are signs of mild hypertension

Hypertension in benign vascular changes occur gradually in response to stable and sustained hypertension. These degenerative changes of the walls of small vessels such as arterioles reduces the effective light with. consequent tissue ischemia, and increased vascular fragility in the brain, with bleeding risk.

In malignant hypertension there is a destruction of the walls of small vessels

When blood pressure rises so much sudden acute destructive changes occur in the walls of small blood vessels, along with remedial proliferative responses in
walls of small arteries. These alterations produced by lack of blood flow to small vessels, with formation of multiple foci of necrosis, eg in renal glomeruli.

High blood pressure affects mainly the heart, brain, kidneys and aorta

The pathological consequences of hypertension are observed mainly in four tissues:
• Heart. With increasing pressure, left ventricular myocardial hypertrophy. Since hypertension is often associated with a greater intensity of atherosclerosis, the coronary flow may be insufficient, and produced a
ischemic heart disease. The left ventricular failure is a normal consequence of hypertensive heart disease.
• Brain. Hypertensive patients are especially prone to intracerebral hemorrhage from ruptured intracerebral blood vessels. The lesion of small vessels of the cerebral hemispheres microinfartos occurs as small areas of brain destruction filled with fluid ( "gaps hypertensive).
• Kidney. The progressive arteriolosclerosis produces ischemia of the nephron, which ends up destroying the glomeruli, and atrophy of the tubular system. The disease progresses slowly, as the injured nephron at a time. When the number of functional nephron by ischemia is not high enough, the patient developed a chronic renal failure slowly
progressive. If hypertension has produced significant ischemia of the nephron, the kidney is said to have suffered a mild hypertensive nefrosclerosis. This is a major cause of kidney failure
Chronic middle and advanced age.
• Aorta. Hypertension predisposes to the development of large abdominal aortic aneurysms and dissections of the mean.

Secondary hypertension is less than 10% of cases

In a minority of cases it is considered that there is any structural alteration responsible for the development of systemic hypertension. For example, stenosis
of the renal artery (usually at its root) may cause atherosclerosis by hypertension, with possible surgical treatment. Hypertension is associated with elevated levels of renin and angiotensin II in the circulation from the ischemic kidney, and can be cured in early stages through
removal of the kidney affection. Hypertension is also a symptom of diffuse nephropathies such as glomerulonephritis and pyelonephritis. Hypertension is transient in the initial acute phase of glomerular diseases (p, ej.,
acute nephritic syndrome), but standing diffuse chronic nephropathies.
Pheochromocytoma, an adrenaline-secreting tumor that arises normally noradrenaline in the adrenal medulla, produces a hypertension that
initially paroxysmal.

The aortic coarctation is a congenital malformation increased peripheral resistance due to a structural stenosis of the aorta. In these cases, systemic hypertension is not really because it only affects the arterial system ahead of the coarctation, usually to the arms, head and neck.

Hypertension is a symptom of diseases of the adrenal cortex that are associated with excessive production of glucocorticoids and mineralocorticoids (Cushing's syndrome and Conn síndromede).

It is also a symptom of preeclampsia, and may be associated with endocrinopathies such as thyrotoxicosis, acromegaly, and sometimes hypothyroidism, or due to a neurogenic causes such as intracranial hypertension.

treatment

a) In patients with hypertension grade I or II, we recommend starting treatment with a single drug. If the patient has hypertension hyperkinetic syndrome, the best option is a beta blocker, it is inconvenient and the use of vasodilators such as alpha blockers or calcium antagonists as exacerbate circulatory hyperkinesia. In patients who are suspected of expanding the extracellular space (especially women) the best option is the diuretic as mono therapy, are less effective than beta blockers and vasodilators are contraindicated deteriorating fluid retention and expansion of the intravascular space. Can be equally effective inhibitors of ACE. In elderly with systolic hypertension is preferable to use calcium antagonists as drugs of first choice.

b) Patients with essential hypertension grade III, requires the use of multiple drugs to achieve an efficient control of hypertension. This form is preferred to initiate treatment with beta blockers and diuretics (thiazides and potassium-sparing). Failure to reach an effective control of blood pressure can add an ACE inhibitor. Where not achieved normalization of blood pressure can be used vasodilators (hydralazine, minoxidil, prazosin) which reduce vascular resistance. The calcium antagonists can be used in such patients are not able to control hypertension with drugs and or because there are two states that suspend their administration by undesirable side effects such as: attack of gout (thiazides), asthma or heart failure ( betablockers) or persistent cough (ACE inhibitors). The anta gonistas calcium can also produce undesirable side effects (edema, facial flushing) that can bind to the suspension or change to another drug of a different family.
As a general conclusion one can say that treatment of hypertensive patient should be individualized taking into account age, clinical conditions and hemodynamic effects of drugs.

c) The patient with grade IV hypertension is a hypertensive emergency or urgency, so that their treatment requires immediate hospitalization and therapy.

Hypertensive crisis

a) The patient was asymptomatic but with figures of diastolic blood pressure of 140 mmHg or greater should be hospitalized for observation and absolute rest, being administered by sublingual nifedipine at 10 mg.

b) The patient with hypertensive crisis, with increased blood pressure of 180/140 and acute pulmonary edema must be treated with Fowler position, sitting on the bed edge, rotating tourniquets, by IV furosemide at a rate between 20 and 60 mg by sodium nitroprusside and IV diluted in dextrose solution at a rate of 0.3 to 8 mg / kg / min, and in some cases these measures achieves jugular table, but others should also scan the patient in a timely manner (or C lanata Ouabain). When the patient is already in clinical conditions will be acceptable to initiate antihypertensive oral.

c) The patient with hypertensive crisis which is associated with hypertensive encephalopathy is presented to the doctor with a very ostentatious manifesting headache, nausea, projectile vomiting, blurred vision and a progressive state of mental obnubilación all this coincides with elevations exaggerated the figures for blood pressure (> 180/140). The appropriate procedure will also be treated with sodium nitropusiato given as mentioned in the previous paragraph, although such cases can also be used diazoxide at a starting dose of 300 mg IV which can be repeated w / 4 or 6 hours, depending on the response. It should be remembered that the prolonged administration of this drug produces sodium and water retention, so when their use is extended for more than 24 hours should join the administration of diuretics. As soon as possible to initiate oral therapy.

d) The hypertensive crisis which is complicated with an aortic dissection is presented as an acute where the patient can present intense chest pain or back accompanied by feelings of death, pallor, diaphoresis, and elevated mind exaggerated figures (> 180/140 mmHg). This table should be treated with sodium nitroprusside, another alternative is alfametildopa drug at a rate of 250 to 500 mg IV c / 4 to 6 hours and has been checked in to start oral antihypertensive therapy.

e) If a hypertensive crisis due to a pheochromocytoma patient relate headache, palpitations and was found with pallor and diaphoresis, sinus tachycardia and excessively high numbers (> 180 / 140 mmHg), in which case the ideal treatment should be done with phentolamine, injected an initial bolus of 5 to 15 mg IV and then on a continuous drip to maintain blood pressure numbers at acceptable levels. If heart rate is exageradeamente high (> 150 per minute) or appear as tachyarrythmia paroxysmal atrial fibrillation by propranolol should be administered by IV at a rate of 1 mg / min up to 3 to 5 mg total dose.

Patients with essential hypertension grade III, requires several drugs to achieve the desired control. In summary, the treatment should be individualized according to age, clinical conditions and hemodynamic sensitivity to drugs.

Prevention methods

* Quitting smoking reduces mortality to half of those who continue to smoke.
* Controlling hypertension.
* Reduction of body weight.
* Increase physical activity.
* Controlling Diabetes
* Changes in eating habits.

The onset may be abrupt, such as acute myocardial infarction or may be a chronic disorder, with increasing loss of functions of the heart. In turn this may be offset a disease where the activity remains normal or decompensated, in which the patient suffers dyspnea and precordial pain in this case should rest and receive medication and diuretics.
From a nutritional point of view it is the implementation of a diet hiposódica (containing less than 5grs. Salt daily).

In coronary disease should avoid foods rich and abundant as they impose an excessive burden on the heart and circulation.

When making a food choice for these patients should be sought to replace the salt and no abdominal distension, constipation and flatulence.

Bibliography:
• Patologia Roobins 2007
• Patologia Rubin
• Web Journal Cardiology hypertensive crisis
• Institute of Cardiology http://www.drscope.com/cardiologia/pac/arterial.htm
• Goodman and Gilman, Farmacologia.
• National Institute of Cardiology - Ignacio Chávez, Hypertension Articles
• National Association of Cardiologists of Mexico
• Society of Interventional Cardiology of Mexico
• National Society of Echocardiography in Mexico
Nutrition zonadiet.com 2004 • Hypertension
• Vascular Health. is
• Book Fisiologia Guyton
• Stevens Patologia

About the Author

Student: School of Medicine Ignacio Santos. Committee member of medical research. Member of the EMC Updates medicas JOURNAL CLUB. Member and Supervisor of medical items since 2007. Member of The Neurology Service On-Line Journal Club. Contributor Renal Pathology MCQs

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