A treatment plan may involve lactulose, enemas, and use of antibiotics such as rifaximin, neomycin, vancomycin, and the quinolones. Restriction of dietary protein was recommended but this is now refuted by a clinical trial which shows no benefit. Instead, the maintenance of adequate nutrition is now advocated.

The management of ascites needs to be gradual to avoid sudden changes in systemic volume status which can precipitate hepatic encephalopathy, renal failure and death. The management includes salt restriction, diuretics (spironolactone), paracentesis, and transjugular intrahepatic portosystemic shunt.

Several classes of antihypertensive agents are recommended, with the choice depending on the cause of the hypertensive crisis, the severity of the elevation in blood pressure, and the usual blood pressure of the person before the hypertensive crisis. In most cases, the administration of intravenous sodium nitroprusside injection which has an almost immediate antihypertensive effect, is suitable (but in many cases not readily available). Besides, nitroprusside runs a risk of cyanide poisoning. Other intravenous agents like nitroglycerine, nicardipine, labetalol, fenoldopam or phentolamine can also be used, but all have a delayed onset of action (by several minutes) compared to sodium nitroprusside.

In addition, non-pharmacological treatment could be considered in cases of resistant malignant hypertension due to end stage kidney failure, such as surgical nephrectomy, laparoscopic nephrectomy, and renal artery embolization in cases of anesthesia risk.

It is also important that the blood pressure is lowered smoothly, not too abruptly. The initial goal in hypertensive emergencies is to reduce the pressure by no more than 25% (within minutes to 1 or 2 hours), and then toward a level of 160/100 mm Hg within a total of 2–6 hours. Excessive reduction in blood pressure can precipitate coronary, cerebral, or renal ischemia and, possibly, infarction.

The diagnosis of a hypertensive emergency is not based solely on an absolute level of blood pressure, but also on the typical blood pressure level of the patient before the hypertensive crisis occurs. Individuals with a history of chronic hypertension may not tolerate a "normal" blood pressure.

Certain medications, including NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension. Other medications include extrogens (such as those found in oral contraceptives with high estrogenic activity), certain antidepressants (such as venlafaxine), buspirone, carbamazepine, bromocriptine, clozapine, and cyclosporine.

High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications is called rebound hypertension. The increases in blood pressure may result in blood pressures greater than when the medication was initiated. Depending on the severity of the increase in blood pressure, rebound hypertension may result in a hypertensive emergency. Rebound hypertension is avoided by gradually reducing the dose (also known as "dose tapering"), thereby giving the body enough time to adjust to reduction in dose. Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine and methyl-dopa.

Other herbal or "natural products" which have been associated with hypertension include ma huang, St John's wort, and licorice.

Regular physical exercise reduces blood pressure. The UK National Health Service advises 150 minutes (2 hours and 30 minutes) of moderate-intensity aerobic activity per week to help prevent hypertension.

The initial aim of treatment in hypertensive crises is to rapidly lower the diastolic pressure to about 100 to 105 mmHg; this goal should be achieved within two to six hours, with the maximum initial fall in BP not exceeding 25 percent of the presenting value. This level of BP control will allow gradual healing of the necrotizing vascular lesions. More aggressive hypotensive therapy is both unnecessary and may reduce the blood pressure below the autoregulatory range, possibly leading to ischemic events (such as stroke or coronary disease).

Once the BP is controlled, the person should be switched to medication by mouth, with the diastolic pressure being gradually reduced to 85 to 90 mmHg over two to three months. The initial reduction to a diastolic pressure of approximately 100 mmHg is often associated with a modest worsening of renal function; this change, however, is typically transient as the vascular disease tends to resolve and renal perfusion improves over one to three months. Antihypertensive therapy should not be withheld in this setting unless there has been an excessive reduction in BP. A change in medication, however, is indicated if the decline in renal function is temporally related to therapy with an angiotensin (ACE) converting enzyme inhibitor or angiotensin II receptor blocker, which can interfere with renal autoregulation and produce acute renal failure in patients with bilateral renal artery stenosis. (See "Renal effects of ACE inhibitors in hypertension".)

Several parenteral antihypertensive agents are most often used in the initial treatment of malignant hypertension.

- Nitroprusside – an arteriolar and venous dilator, given as an intravenous infusion. Nitroprusside acts within seconds and has a duration of action of only two to five minutes. Thus, hypotension can be easily reversed by temporarily discontinuing the infusion, providing an advantage over the drugs listed below. However, the potential for cyanide toxicity limits the prolonged use of nitroprusside, particularly in patients with renal insufficiency.

- Nicardipine – an arteriolar dilator, given as an intravenous infusion.

- Clevidipine – a short-acting dihydropyridine calcium channel blocker. It reduces blood pressure without affecting cardiac filling pressures or causing reflex tachycardia.

- Labetalol – an alpha- and beta-adrenergic blocker, given as an intravenous bolus or infusion. Bolus followed by infusion.

- Fenoldopam – a peripheral dopamine-1 receptor agonist, given as an intravenous infusion.

- Oral agents — A slower onset of action and an inability to control the degree of BP reduction has limited the use of oral antihypertensive agents in the therapy of hypertensive crises. They may, however, be useful when there is no rapid access to the parenteral medications described above. Both sublingual nifedipine and sublingual captopril can substantially lower the BP within 10 to 30 minutes in many patients. A more rapid response is seen when liquid nifedipine is swallowed.

The major risk with oral agents is ischemic symptoms (e.g., angina pectoris, myocardial infarction, or stroke) due to an excessive and uncontrolled hypotensive response. Thus, their use should generally be avoided in the treatment of hypertensive crises if more controllable drugs are available.

Prostacyclin (prostaglandin I) is commonly considered the most effective treatment for PAH. Epoprostenol (synthetic prostacyclin) is given via continuous infusion that requires a semi-permanent central venous catheter. This delivery system can cause sepsis and thrombosis. Prostacyclin is unstable, and therefore has to be kept on ice during administration. Since it has a half-life of 3 to 5 minutes, the infusion has to be continuous, and interruption can be fatal. Other prostanoids have therefore been developed. Treprostinil can be given intravenously or subcutaneously, but the subcutaneous form can be very painful. An increased risk of sepsis with intravenous Remodulin has been reported by the CDC. Iloprost is also used in Europe intravenously and has a longer half life. Iloprost was the only inhaled form of prostacyclin approved for use in the US and Europe, until the inhaled form of treprostinil was approved by the FDA in July 2009.

Many pathways are involved in the abnormal proliferation and contraction of the smooth muscle cells of the pulmonary arteries in patients with pulmonary arterial hypertension. Three of these pathways are important since they have been targeted with drugs — endothelin receptor antagonists, phosphodiesterase type 5 (PDE-5) inhibitors, and prostacyclin derivatives.

In general, the treatment of PPH is derived from the treatment of pulmonary hypertension. The best treatment available is the combination of medical therapy and liver transplantation.

The ideal treatment for PPH management is that which can achieve pulmonary vasodilatation and smooth muscle relaxation without exacerbating systemic hypotension. Most of the therapies for PPH have been adapted from the primary pulmonary hypertension literature. Calcium channel blockers, b-blockers and nitrates have all been used – but the most potent and widely used aids are prostaglandin (and prostacyclin) analogs, phosphodiesterase inhibitors, nitric oxide and, most recently, endothelin receptor antagonists and agents capable of reversing the remodeling of pulmonary vasculature.

Inhaled nitric oxide vasodilates, decreasing pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) without affecting systemic artery pressure because it is rapidly inactivated by hemoglobin, and improves oxygenation by redistributing pulmonary blood flow to ventilated areas of lung. Inhaled nitric oxide has been used successfully to bridge patients through liver transplantation and the immediate perioperative period, but there are two significant drawbacks: it requires intubation and cannot be used for long periods of time due to methemoglobinemia.

Prostaglandin PGE1 (Alprostadil) binds G-protein linked cell surface receptors that activate adenylate cyclase to relax vascular smooth muscle. Prostacyclin – PGI2, an arachadonic acid derived lipid mediator (Epoprostenol, Flolan, Treprostenil) – is a vasodilator and, at the same time, the most potent inhibitor of platelet aggregation. More importantly, PGI2 (and not nitrous oxide) is also associated with an improvement in splanchnic perfusion and oxygenation. Epoprostenol and ilioprost (a more stable, longer acting variation) can and does successfully bridge for patients to transplant. Epoprostenol therapy can lower PAP by 29-46% and PVR by 21-71%., Ilioprost shows no evidence of generating tolerance, increases cardiac output and improves gas exchange while lowering PAP and PVR. A subset of patients does not respond to any therapy, likely having fixed vascular anatomic changes.

Phosphodiesterase inhibitors (PDE-i) have been employed with excellent results. It has been shown to reduce mean PAP by as much as 50%, though it prolongs bleeding time by inhibiting collagen-induced platelet aggregation. Another drug, Milrinone, a Type 3 PDE-i increases vascular smooth muscle adenosine-3,5-cyclic monophosphate concentrations to cause selective pulmonary vasodilation. Also, by causing the buildup of cAMP in the myocardium, Milrinone increases contractile force, heart rate and the extent of relaxation.

The newest generation in PPH pharmacy shows great promise. Bosentan is a nonspecific endothelin-receptor antagonist capable of neutralizing the most identifiable cirrhosis associated vasoconstrictor, safely and efficaciously improving oxygenation and PVR, especially in conjunction with sildenafil. Finally, where the high pressures and pulmonary tree irritations of PPH cause a medial thickening of the vessels (smooth muscle migration and hyperplasia), one can remove the cause –control the pressure, transplant the liver – yet those morphological changes persist, sometimes necessitating lung transplantation. Imatinib, designed to treat chronic myeloid leukemia, has been shown to reverse the pulmonary remodeling associated with PPH.

Several treatment options have been developed for portal hypertensive gastropathy. The first is the use of beta-blockers, which reduce portal pressures. Non-selective beta blockers (such as propranolol and nadolol) have been used to decrease the pressure of the portal vein in patients with esophageal varices, and have been shown to regress portal hypertensive gastropathy that has been worsened by medical treatment of varices. Propranolol has also been evaluated in patients with chronic cirrhosis and portal hypertensive gastropathy. Other medications that primarily treat bleeding, including anti-fibrinolytic medications such as tranexamic acid have also been used in case reports of patients with portal hypertensive gastropathy. These medications work by stabilizing deposits of fibrin at sites that ordinarily would bleed.

Finally, octreotide, an analogue of somatostatin that leads to vasoconstriction of the portal circulation, can be used for active bleeding due to portal hypertensive gastropathy. Sucralfate, a coating medication has also been used, but evidence is from animal models.

Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.

It has been suggested that vitamin D deficiency is associated with cardiovascular risk factors. 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.

Also, some authorities claim that potassium might both prevent and treat hypertension.

Patients with hypertensive encephalopathy who are promptly treated usually recover without deficit. However, if treatment is not administered, the condition can lead to death.

The aim of the medical treatment is to slow the progression of chronic kidney disease by reducing blood pressure and albumin levels. The current published guidelines define ideal BP of <130/80 mmHg for patients with hypertensive nephropathy; studies show that anything higher or lower than this can increase cardiovascular risk. According to the African American Study of Kidney Disease (AASK) trial, after an additional 5 years follow-up upon completion of the 10-year trial, up to 65% of the cohort had progressive nephropathy despite having controlled the mean systolic BP level <135 mmHg.

ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors and aldosterone antagonists, are pharmacological treatments that can be used to lower BP to target levels; hence reducing neuropathy and proteinuria progression. The management plan should be individualized based on the condition of the patients including comorbidities and previous medical history.

In addition, there are lifestyle changes that can be made. Weight reduction, exercise, reducing salt intake can be done to manage hypertensive nephropathy.

Portal hypertensive gastropathy can also be treated with endoscopic treatment delivered through a fibre-optic camera into the stomach. Argon plasma coagulation and electrocautery have both been used to stop bleeding from ectatic vessels, and to attempt to obliterate the vessels, but have limited utility if the disease is diffuse.

Transjugular intrahepatic portosystemic shunt procedures, or TIPS involve decompressing the portal vein by shunting a portal venule to a lower pressure systemic venule, under guidance with fluoroscopy. Since it treats the root cause of portal hypertension gastropathy, it has been putatively used for the condition. The literature reports suggest both regression of portal hypertensive gastropathy on endoscopic images and improvement in bleeding after TIPS.

Finally, cryotherapy involves the use of pressurized carbon dioxide administered through the endoscope to freeze and destroy tissue in a focal area. It is being studied for the treatment of portal hypertensive gastropathy.

At present, there is no effective specific treatment available for diabetic cardiomyopathy. Treatment centers around intense glycemic control through diet, oral hypoglycemics and frequently insulin and management of heart failure symptoms. There is a clear correlation between increased glycemia and risk of developing diabetic cardiomyopathy, therefore, keeping glucose concentrations as controlled as possible is paramount. Thiazolidinediones are not recommended in patients with NYHA Class III or IV heart failure secondary to fluid retention.

As with most other heart diseases, ACE inhibitors can also be administered. An analysis of major clinical trials shows that diabetic patients with heart failure benefit from such a therapy to a similar degree as non-diabetics. Similarly, beta blockers are also common in the treatment of heart failure concurrently with ACE inhibitors.

The medical care of patients with hypertensive heart disease falls under 2 categories—

- Treatment of hypertension

- Prevention (and, if present, treatment) of heart failure or other cardiovascular disease

As previously stated, management of HFpEF is primarily dependent on the treatment of symptoms and exacerbating conditions. Currently treatment with ACE inhibitors, calcium channel blockers, beta blockers, and angiotensin receptor blockers are employed but do not have a proven benefit in HFpEF patients. Additionally, use of Diuretics or other therapies that can alter loading conditions or blood pressure should be used with caution. It is not recommended that patients be treated with phosphodiesterase-5-inhibitors or digoxin.

Antimineralocorticoid is currently recommended for patients with HFpEF who show elevated brain natriuretic peptide levels. Spironolactone is the first member of this drug class and the most frequently employed. Care should be taken to monitor serum potassium levels as well as kidney function, specifically glomerular filtration rate during treatment.

Beta blockers play a rather obscure role in HFpEF treatment but appear to play a beneficial role in patient management. There is currently a deficit of clinical evidence to support a particular benefit for HFpEF patients, with most evidence resulting from HFpEF patients' inclusion in broader heart failure trials. However, some evidence suggests that vasodilating beta blockers, such as nebivolol, can provide a benefit for patients with heart failure regardless of ejection fraction. Additionally, because of the chronotropic perturbation and diminished LV filling seen in HFpEF the bradycardic effect of beta blockers may enable improved filling, reduced myocardial oxygen demand and lowered blood pressure. However, this effect also can contribute to diminished response to exercise demands and can result in an excessive reduction in heart rate.

ACE inhibitors do not appear to improve morbidity or mortality associated with HFpEF alone. However, they are important in the management of hypertension, a significant player in the pathophysiology of HFpEF.

Angiotensin II receptor blocker treatment shows an improvement in diastolic dysfunction and hypertension that is comparable to other anti-hypertensive medication.

According to JNC 7, BP goals should be as follows :

- Less than 140/90mm Hg in patients with uncomplicated hypertension

- Less than 130/85mm Hg in patients with diabetes and those with renal disease with less than 1g/24-hour proteinuria

- Less than 125/75mm Hg in patients with renal disease and more than 1 g/24-hour proteinuria

Secondary hypertension results from an identifiable cause. Kidney disease is the most common secondary cause of hypertension. Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, renal artery stenosis (from atherosclerosis or fibromuscular dysplasia), hyperparathyroidism, and pheochromocytoma. Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive eating of liquorice, excessive drinking of alcohol, and certain prescription medicines, herbal remedies, and illegal drugs such as cocaine and methamphetamine. Arsenic exposure through drinking water has been shown to correlate with elevated blood pressure.

Hypertension (HTN or HT), also known as high blood pressure (HBP), is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure usually does not cause symptoms. Long-term high blood pressure, however, is a major risk factor for coronary artery disease, stroke, heart failure, peripheral vascular disease, vision loss, chronic kidney disease, and dementia.

High blood pressure is classified as either primary (essential) high blood pressure or secondary high blood pressure. About 90–95% of cases are primary, defined as high blood pressure due to nonspecific lifestyle and genetic factors. Lifestyle factors that increase the risk include excess salt in the diet, excess body weight, smoking, and alcohol use. The remaining 5–10% of cases are categorized as secondary high blood pressure, defined as high blood pressure due to an identifiable cause, such as chronic kidney disease, narrowing of the kidney arteries, an endocrine disorder, or the use of birth control pills.

Blood pressure is expressed by two measurements, the systolic and diastolic pressures, which are the maximum and minimum pressures, respectively. For most adults, normal blood pressure at rest is within the range of 100–130 millimeters mercury (mmHg) systolic and 60–80 mmHg diastolic. For most adults, high blood pressure is present if the resting blood pressure is persistently at or above 130/90 or 140/90 mmHg. Different numbers apply to children. Ambulatory blood pressure monitoring over a 24-hour period appears more accurate than office-based blood pressure measurement.

Lifestyle changes and medications can lower blood pressure and decrease the risk of health complications. Lifestyle changes include weight loss, decreased salt intake, physical exercise, and a healthy diet. If lifestyle changes are not sufficient then blood pressure medications are used. Up to three medications can control blood pressure in 90% of people. The treatment of moderately high arterial blood pressure (defined as >160/100 mmHg) with medications is associated with an improved life expectancy. The effect of treatment of blood pressure between 130/80 mmHg and 160/100 mmHg is less clear, with some reviews finding benefit and others finding unclear benefit. High blood pressure affects between 16 and 37% of the population globally. In 2010 hypertension was believed to have been a factor in 18% of all deaths (9.4 million globally).

In a hypertensive urgency blood pressure should be lowered carefully to ≤160/≤100 mmHg over a period of hours to days, this can often be done as an outpatient. There is limited evidence regarding the most appropriate rate of blood pressure reduction, although it is recommended that mean arterial pressure should be lowered by no more than 25 to 30 percent over the first few hours. There is also limited evidence about the best drugs in hypertensive urgencies, oral, short-acting agent such as captopril, labetalol, or clonidine have been used. Sublingual nifedipine is contraindicated in hypertensive urgencies and should "not" be used. Acute administration of drugs should be followed by several hours of observation to ensure that blood pressure does not fall too much. Aggressive dosing with intravenous drugs or oral agents which lowers blood pressure too rapidly carries risk; conversely there is no evidence that failure to rapidly lower blood pressure in a hypertensive urgency is associated with any increased short-term risk.

Despite increasing incidence of HFpEF effective inroads to therapeutics have been largely unsuccessful. Currently, recommendations for treatment are directed at symptom relief and co-morbid conditions. Frequently this involves administration of diuretics to relieve complications associated with volume overload, such as leg swelling and high blood pressure.

Commonly encountered conditions that must be treated for and have independent recommendations for standard of care include atrial fibrillation, coronary artery disease, hypertension, and hyperlipidemia. There are particular factors unique to HFpEF that must be accounted for with therapy. Unfortunately, currently available randomized clinical trials addressing the therapeutic adventure for these conditions in HFpEF present conflicting or limited evidence.

Specific aspects of therapeutics should be avoided in HFpEF to prevent the deterioration of the condition. Considerations that are generalizable to heart failure include avoidance of a fast heart rate, elevations in blood pressure, development of ischemia, and atrial fibrillation. More specific to HFpEF include avoidance of preload reduction. As patients display normal ejection fraction but reduced cardiac output they are especially sensitive to changes in preloading and may rapidly display signs of output failure. This means administration of diuretics and vasodilators must be monitored carefully.

HFrEF and HFpEF represent distinct entities in terms of development and effective therapeutic management. Specifically cardiac resynchronization, administration of beta blockers and angiotensin converting enzyme inhibitors are applied to good effect in HFrEF but are largely ineffective at reducing morbidity and mortality in HFpEF. Many of these therapies are effective in reducing the extent of cardiac dilation and increasing ejection fraction in HFrEF patients. It is unsurprising they fail to effect improvement in HFpEF patients, given their un-dilated phenotype and relative normal ejection fraction. Understanding and targeting mechanisms unique to HFpEF are thus essential to the development of therapeutics.

Randomized studies on HFpEF patients have shown that exercise improves left ventricular diastolic function, the heart's ability to relax, and is associated with improved aerobic exercise capacity. The benefit patients seem to derive from exercise does not seem to be a direct cardiac effect but rather is due to changes in peripheral vasculature and skeletal muscle, which show abnormalities in HFpEF patients.

Patients should be regularly assessed to determine progression of the condition, response to interventions, and need for alteration of therapy. Ability to perform daily tasks, hemodynamic status, kidney function, electrolyte balance, and serum natriuretic peptide levels are important parameters. Behavioral management is important in these patients and it is recommended that individuals with HFpEF avoid alcohol, smoking, and high sodium intake.

Severe hypertension is a serious and potentially life-threatening medical condition. It is estimated that people who do not receive appropriate treatment only live an average of about three years after the event.

The morbidity and of hypertensive emergencies depend on the extent of end-organ dysfunction at the time of presentation and the degree to which blood pressure is controlled afterward. With good blood pressure control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.

The risks of developing a life-threatening disease affecting the heart or brain increase as the blood flow increases. Commonly, ischemic heart attack and stroke are the causes that lead to death in patients with severe hypertension. It is estimated that for every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.

Several studies have concluded that African Americans have a greater incidence of hypertension and a greater morbidity and mortality from hypertensive disease than non-Hispanic whites. It appears that hypertensive crisis is also more common in African Americans compared with other races.

Although severe hypertension is more common in the elderly, it may occur in children (though very rarely). Also, women have slightly increased risks of developing hypertension crises than do men. The lifetime risk for developing hypertension is 86-90% in females and 81-83% in males.

Surgical treatment is best, when it can be performed. Pressure within the portal vein is measured as the shunt is closed, and it must be kept below 20 cm HO or else portal hypertension will ensue. Methods of shunt attenuation should aim to slowly occlude the vessel over several weeks to months in order to avoid complications associated with portal hypertension. These methods include ameroid ring constrictors, cellophane banding, intravascular or percutaneous silicone hydraulic occluders. The most common methods of attenuation used by veterinarians are ameroid ring constrictors and cellophane banding. Both methods have reportedly good outcomes in both cats and dogs, although the true composition of readily sourced cellophane has been found to be made from plastics (inert) and not cellulose (stimulates a fibrous reaction). Recently, a commercial supplier of regenerated cellulose based cellophane for veterinarians has been established for use of cellophane banding for portosystemic shunts in dogs and cats. Complete closure of extrahepatic shunts results in a very low recurrence rate, while incomplete closure results in a recurrence rate of about 50 percent. However, not all dogs with extrahepatic shunts tolerate complete closure (16 to 68 percent). Intrahepatic shunts are much more difficult to surgically correct than extrahepatic shunts due to their hidden nature, large vessel size, and greater tendency toward portal hypertension when completely closed. When surgery is not an option, PSS is treated as are other forms of liver failure. Dietary protein restriction is helpful to lessen signs of hepatic encephalopathy, and antibiotics such as neomycin or metronidazole and other medicines such as lactulose can reduce ammonia production and absorption in the intestines. The prognosis is guarded for any form of PSS.