Hypertension

INTRODUCTION

Hypertension is one of the most common worldwide diseases afflicting humans. Because of the associated morbidity and mortality and the cost to society, hypertension is an important public health challenge. Over the past several decades, extensive research, widespread patient education, and a concerted effort on the part of health care professionals have led to decreased mortality and morbidity rates from the multiple organ damage arising from years of untreated hypertension. Hypertension is the most important modifiable risk factor for coronary heart disease (the leading cause of death in North America), stroke (the third leading cause), congestive heart failure, end-stage renal disease, and peripheral vascular disease. Therefore, health care professionals must not only identify and treat patients with hypertension but also promote a healthy lifestyle and preventive strategies to decrease the prevalence of hypertension in the general population.

•    Pre-hypertension – Systolic blood pressure (SBP) 120-139 or diastolic blood pressure(DBP) 80-89
•    Stage I HTN – SBP 140-159 or DBP 90-99
•    Stage II HTN – SBP >160 or DBP >100

Hypertensive crises encompass a spectrum of clinical presentations where uncontrolled BPs leads to progressive or impending target organ dysfunction (TOD). The clinical distinction between hypertensive emergencies and hypertensive urgencies depends on the presence of acute TOD and not on the absolute level of the BP.

Hypertensive emergencies represent severe HTN with acute impairment of an organ system (eg, central nervous system [CNS], cardiovascular, renal). In these conditions, the BP should be lowered aggressively over minutes to hours.

Hypertensive urgency is defined as a severe elevation of BP, without evidence of progressive target organ dysfunction. These patients require BP control over several days to weeks.

Causes
The most common hypertensive urgency is a rapid unexplained rise in BP in a patient with chronic essential HTN.

Other causes:

  • Renal parenchymal disease – Chronic pyelonephritis, primary glomerulonephritis, tubulointerstitial nephritis (accounts for 80% of all  secondary causes)
  • Systemic disorders with renal involvement – Systemic lupus erythematosus, systemic sclerosis,  vasculitides
  • Renovascular disease – Atherosclerotic disease, fibromuscular dysplasia, polyarteritis nodosa
  • Endocrine – Pheochromocytoma, Cushing syndrome, primary hyperaldosteronism
  • Drugs – Cocaine, amphetamines, cyclosporin, clonidine withdrawal, phencyclidine, diet pills, oral contraceptive pills
  • Drug interactions – Monoamine oxidase inhibitors with tricyclic antidepressants, antihistamines, or  tyramine-containing food
  • CNS – CNS trauma or spinal cord disorders, such as Guillain-Barré syndrome
  • Coarctation of the aorta
  • Preeclampsia/eclampsia
  • Postoperative hypertension

Physical

Vitals

  • BP should be measured in both the supine position and the standing position (assess volume depletion).
  • BP should also be measured in both arms (a significant difference suggests an aortic dissection).

ENT: The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive urgency.

Cardiovascular – Evaluate for the presence of heart failure.

  • Jugular venous distension
  • Crackles
  • Peripheral edema

Abdomen – Abdominal masses or bruits
CNS

  • Level of consciousness
  • Visual fields
  • Focal neurologic signs

Takayasu arteritis is a granulomatous vasculitis of unknown etiology that commonly affects the thoracic and abdominal aorta. It causes intimal fibroproliferation of the aorta, great vessels, pulmonary arteries, and renal arteries and results in segmental stenosis, occlusion, dilatation, and aneurysmal formation in these vessels. Takayasu arteritis is the only form of aortitis that causes stenosis and occlusion of the aorta.

Takayasu disease has also been referred to as pulseless disease and aortic arch syndrome. During the acute inflammatory stage, Takayasu disease causes a low-grade temperature, tachycardia, pain adjacent to the inflamed arteries (eg, carotodynia), and easy fatigability in 50% of patients. Carotid and clavicular bruits, asymmetric upper-extremity blood pressures, hypertension, diminished or absent upper-extremity pulses, and ischemic symptoms can suggest the diagnosis

ANATOMY & PHYSIOLOGY

Central Nervous System

Medulla Oblongata; relays motor and sensory impulses between other parts of the brain and the spinal cord. Reticular formation (also in pons, midbrain, and diencephalon) functions in consciousness and arousal. Vital centers regulate heartbeat, breathing (together with pons) and blood vessel diameter.

Hypothalamus; controls and intergrates activities of the autonomic nervous system and pituitary gland. Regulates emotional and behavioral patterns and circadian rhythms. Controls body temperature and regulates eating and drinking behavior. Helps maintain the waking state and establishes patterns of sleep. Produces the hormones oxytocin and antidiuretic hormone.

Cardiovascular System

Baroreceptor, pressure-sensitive sensory receptors, are located in the aorta, internal carotid arteries, and other large arteries in the neck and chest. They send impulses to the cardiovascular center in the medulla oblongata to help regulate blood pressure. The two most important baroreceptor reflexes are the carotid sinus reflex and the aortic reflex.

Chemoreceptors, sensory receptors that monitor the xhemical composition of blood, are located close to the baroreceptors of the carotid sinus and the arch of the aorta in small structures called carotid bodies and aortic bodies, respectively. These chemoreceptors detect changes in blood level of O2, CO2, and H+.

Renal System

Renin-Angiotensin-Aldosterone
system. When blood volume falls or blood flow to the kidneys decreases, juxtaglomerular cells in the kidneys secrete renin into the bloodstream. In sequence, renin and angiotensin converting enzyme (ACE) act on their substrates to produce the active hormone angiotensin II, which raises blood pressure in two ways. First, angiotensin II is a potent vasoconstrictor; it raises blood pressure by increasing systemic vascular resistance. Second, it stimulates secretion of aldosterone, which increases reabsorption of sodium ions and water by the kidneys. The water reabsorption increases total blood volume, which increases blood pressure.

Antidiuretic hormone. ADH is produced by the hypothalamus and released from the posterior pituitary in response to dehydration or decreased blood volume. Among other actions, ADH causes vasoconstriction, which increases blood pressure.

Atrial Natriuretic Peptide. Released by cells in the atria of the heart, ANP lowers blood pressure by causing vasodilation and by promoting the loss of salt and water in the urine, which reduces blood volume.

NURSING ASSESSMENT

Present Health History

The present health history started 7 days prior to confinement at PCMC when the patient, experienced general body weakness, vomiting and elevated blood pressure. She was admitted at Duque’s Clinic for 3 days but no BP monitoring was done. After 3 days, she was transferred to Cabiao General Hospital. Chest x-ray was done and the result implies cardiomegaly. She stayed at the said institution for 2 days and was treated as a case of hypertension. The patient was referred to Nueva Ecija Doctors last April 10, she had undergone ultrasound of her abdomen. She was given furosemide, nifedipine, mefenamic acid and ranitidine as her medication. Last April 12, 2007 at 12:55am she was admitted at the Philippine Children’s Medical Center with a diagnosis of Hypertensive Urgency secondary to Takayasu disease.

Past Health History

Prior to her hospitalization , she denies in having any record or medical history of being admitted due to trauma, accident and disease. She also denies having allergies to food and drugs.

Family Health History

The patient has family health history of hypertension on her mother’s side.

Demographic Data/Physical Assessment & General Appearance

Review of Systems

? Psychosocial
Being the second among three children, she considers herself as an active individual who is fond of interacting with other people. She considers herself as friendly even at home and at work. She excels in her subjects especially in Mathematics.

? Elimination
Her elimination pattern has somehow deviated from her usual urine and stool elimination. Before her confinement, she usually urinates for 7 times a day and defecates at least 2 times per day. During her confinement, she now urinates 4 times a day and defecates once a day. According to her the variation from her elimination pattern is due to change in appetite and setting.

? Rest & Activity
A typical day to her would be waking up at around 7:00 am to eat breakfast and play with her siblings. She had is fond of playing in their neighborhood and running around their house. Her usual sleeping hours is at 8:00 pm. During her confinement, she was not able to rest and have enough sleep as well. During her leisure time before confinement, she loves to watch television.

? Safety
She usually stays at home and around their vicinity when playing. There is no physical threat for her safety.

? Oxygenation
According to her, before and during her confinement she had no difficulty in breathing and ventilation.

? Nutrition
According to her mother, she has a good appetite. She prefers to eat fish and vegetables rather than meat. She also adds that her daughter prefers to drink water.

PATHOPHYSIOLOGY

LABORATORY DIAGNOSIS

MEDICAL & SURGICAL MANAGEMENT

There are three clinical indications for selecting a patient with a hemodynamically significant renal artery stenosis (RAS) for treatment. The first is hypertension that is poorly controlled on adequate (two or three drugs) medical therapy, or in a patient intolerant of hypertensive medications. The second is renal insufficiency, and the third is a “cardiac disturbance” syndrome, such as “flash” pulmonary edema.

The treating physician should have a high clinical suspicion that the target RAS is causally related to the clinical symptoms. The procedural risks, potential benefits, and alternative therapies must be considered for each patient. Generally, a RAS of <50% does not require revascularization, while a symptomatic patient with a stenosis ?70% generally merits revascularization. Absolute criteria for determining lesion severity have not been established; however, a systolic translesional pressure gradient of ?20 mm Hg or a mean gradient of ?10 mm Hg is generally accepted as representing significant renal artery obstruction in symptomatic patients.

Stents are superior to balloons for both procedural success and long-term patency, due to scaffolding of the arterial lumen. The single, randomized, controlled trial comparing stents to balloons in renovascular hypertension demonstrated procedural superiority, better patency rates, and cost-effectiveness for primary stent placement.

Despite a uniformly high (?95%) technical success rate for renal artery stent placement, very few patients will be cured of hypertension. However, the majority of hypertensive patients will benefit by improved blood pressure control and/or the need for fewer medications. Patients with the highest pretreatment systolic blood pressures have the greatest decrease in systolic pressure. A multivariate logistic regression analysis demonstrated that bilateral RAS and mean arterial pressure >110 mm Hg predicted a better blood pressure response following stent placement.

Studies comparing the results in elderly (?75 years) versus younger (<75 years) patients or in females versus males have failed to show any difference in response to renal stent placement. The suggestion that a high level of resistance in the segmental renal arteries (resistance index ?80), determined by noninvasive Doppler measurement, predicted a poor response to revascularization has been challenged by more recent data that suggested that patients with increased resistance respond favorably to renal intervention.

The benefits of renal stent placement include reperfusion of the ischemic kidney(s), resulting in a reduction in the stimulus to renin production, which decreases angiotensin and aldosterone production, thereby decreasing peripheral arterial vasoconstriction and intravascular volume. Improving renal perfusion enhances glomerular filtration, thus natriuresis. Finally, in patients with a solitary kidney or bilateral RAS, the administration of angiotensin antagonists is facilitated by revascularization.

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