Hypertension is a major cause of cerebrovascular accident, cardiac disease, and renal failure. Prognosis is good if this disorder is detected early and treatment begins before complications develop. Severely elevated blood pressure or hypertensive crisis may be fatal.

There is no single identifiable cause of essential hypertension. This condition probably reflects an interaction of multiple homeostatic forces, including changes in renal regulation of sodium and extracellular fluids, in aldosterone secretion and metabolism, and in norepinephrine secretion and metabolism.

Hypertensive crisis, on the other hand, is an acute, life-threatening rise in blood pressure (diastolic usually over 120 mmHg). It may develop in hypertensive patients after abrupt discontinuation of anti-hypertensive medication, increased salt consumption, increased production of rennin, epinephrine, and norepinephrine, and added stress. This emergency requires immediate and vigorous treatment to lower blood pressure and thereby prevent cerebrovascular accident, left heart failure, and pulmonary edema.

Hypertensive crisis produces severe and widespread symptoms, including headache, drowsiness, mental clouding, vomiting, focal neurologic signs (such as paresthesias), and, if pulmonary edema is present, shortness of breath and hemoptysis. Treatment to rapidly lower blood pressure and thereby prevent hypertensive encephalopathy may include vasodilators, such as I.V. nitroprusside, hydralazine, or diaxozide; a potent diuretic, such as furosemide; and a symphathetic blocker, such as methyldopa, trimethaphan, or phentolamine.

In the early stages of antihypertensive I.V. therapy, blood pressure and heart rate should be monitored frequently (as often as one to three minutes with some drugs) for a precipitous drop which indicates hypersensitivity to the prescribed medications. Blood pressure level should be maintained as ordered.

Although hypertension has no cure, drugs and modifications in diet and lifestyle can control it. Drug therapy usually begins with a diuretic alone. Beta- adrenergic blockers, other sympathetic blockers, or vasodilators may be added as needed. Therapy may also include angiotensin-converting enzyme and calcium channel blockers. Lifestyle and dietary changes may include weight loss, relaxation techniques, regular exercise, and restriction of sodium and saturated fat intake.

To encourage compliance with antihypertensive therapy, it should be suggested that the patient establish a daily routine for taking medication. Patient should be warned that uncontrolled hypertension may cause stroke and heart attack. Patient should also be taught to report drug side effects.

Portal hypertension of the elevated pressure in the portal vein occurs when blood flow meets increased resistance. The disorder is a common result of cirrhosis but may also stem from mechanical obstruction and occlusion of the hepatic veins (Budd-Chiari syndrome). As portal pressure rises, blood backs up into the spleen and flows through collateral channels to the venous system, bypassing the liver. Consequently, portal hypertension produces splenomegaly (enlargement of the spleen) with thrombocytopenia, dilated collateral veins (esophageal varices, hemorrhoids, or prominent abdominal veins), and ascites. Nevertheless, in many patients the first sign of portal hypertension is bleeding from the esophageal varices — dilated tortuous veins in the submucosa of the lower esophagus. Such varices often cause massive hematemesis (blood in the vomitus), requiring emergency treatment to control hemorrhage and prevent hypovolemic shock.

Endoscopy identifies the ruptured varix as the bleeding site and excludes other potential sources in the upper GI tract. Angiography may aid diagnosis but is less precise than endoscopy. Vasopressin infused into the superior mesenteric artery may temporarily stop bleeding; when angiography is unavailable, vasopressin may be infused by I.V. drip, diluted with 5% dextrose in water (except in patients with coronary vascular disease), but this route is usually less effective. A Minnesota or Sengstaken-Blakemore tube may also help control hemorrhage by applying pressure on the bleeding site. Iced saline lavage through the tube may help control bleeding.

The use of vasopressin or Minnesota or Sengstaken-Blakemore tube is a temporary measure, especially in the patient with severely deteriorated. Fresh blood and fresh frozen plasma, if available, are preferred for blood transfusions, to replace clotting factors. Treatment with lactulose promotes elimination of old blood from the GI tract and combats excessive production and accumulation of ammonia.

Appropriate surgical bypass procedures include portosystemic anastomosis, splenorenal shunt, and mesocaval shunt. Emergency shunts carry a mortality of 25% to 50%. Clinical evidence suggests that portosystemic bypass does not prolong the patient’s survival time; however, he will eventually die of hepatic coma rather than of hemorrhage.
Care for the patient who has portal hypertension with esophageal varices focuses on careful monitoring for signs and symptoms of hemorrhage and subsequent hypotension, compromised oxygen supply, and altered level of consciousness.