The prognosis of pulmonary arterial hypertension (WHO Group I) has an "untreated" median survival of 2–3 years from time of diagnosis, with the cause of death usually being right ventricular failure (cor pulmonale). A recent outcome study of those patients who had started treatment with bosentan (Tracleer) showed that 89% patients were alive at 2 years. With new therapies, survival rates are increasing. For 2,635 patients enrolled in The Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management (REVEAL Registry) from March 2006 to December 2009, 1-, 3-, 5-, and 7-year survival rates were 85%, 68%, 57%, and 49%, respectively. For patients with idiopathic/familial PAH, survival rates were 91%, 74%, 65%, and 59%. Levels of mortality are very high in pregnant women with severe pulmonary arterial hypertension (WHO Group I). Pregnancy is sometimes described as contraindicated in these women.

The epidemiology of IPAH is about 125–150 deaths per year in the U.S., and worldwide the incidence is similar to the U.S. at 4 cases per million. However, in parts of Europe (France) indications are 6 cases per million of IPAH. Females have a higher incidence rate than males (2–9:1).

Other forms of PH are far more common. In systemic scleroderma, the incidence has been estimated to be 8 to 12% of all patients; in rheumatoid arthritis it is rare. However, in systemic lupus erythematosus it is 4 to 14%, and in sickle cell disease, it ranges from 20 to 40%. Up to 4% of people who suffer a pulmonary embolism go on to develop chronic thromboembolic disease including pulmonary hypertension. A small percentage of patients with COPD develop pulmonary hypertension with no other disease to explain the high pressure. On the other hand, obesity-hypoventilation syndrome is very commonly associated with right heart failure due to pulmonary hypertension.

CTEPH is an orphan disease with an estimated incidence of 5 cases per million, but it is likely that CTEPH is under-diagnosed as symptoms are non-specific. Although a cumulative incidence of CTEPH between 0.1% and 9.1% within the first 2 years after a symptomatic PE has been reported, it is currently unclear whether acute symptomatic PE begets CTEPH. Routine screening for CTEPH after PE is not recommended because a significant number of CTEPH cases develops in the absence of previous acute symptomatic PE. In addition, approximately 25% of patients with CTEPH do not present with a clinical history of acute PE. The median age of patients at diagnosis is 63 years (there is a wide age range, but paediatric cases are rare), and both genders are equally affected.

Historically the prognosis for patients with untreated CTEPH was poor, with a 5-year survival of 40 mmHg at presentation. More contemporary data from the European CTEPH registry have demonstrated a 70% 3-year survival in patients with CTEPH who do not undergo the surgical procedure of pulmonary endarterectomy (PEA). Recent data from an international CTEPH registry demonstrate that mortality in CTEPH is associated with New York Heart Association (NYHA) functional class IV, increased right atrial pressure, and a history of cancer. Furthermore, comorbidities such as coronary disease, left heart failure, and chronic obstructive pulmonary disease (COPD) are risk factors for mortality.

Following diagnosis, mean survival of patients with PPH is 15 months. The survival of those with cirrhosis is sharply curtailed by PPH but can be significantly extended by both medical therapy and liver transplantation, provided the patient remains eligible.

Eligibility for transplantation is generally related to mean pulmonary artery pressure (PAP). Given the fear that those PPH patients with high PAP will suffer right heart failure following the stress of post-transplant reperfusion or in the immediate perioperative period, patients are typically risk-stratified based on mean PAP. Indeed, the operation-related mortality rate is greater than 50% when pre-operative mean PAP values lie between 35 and 50 mm Hg; if mean PAP exceeds 40-45, transplantation is associated with a perioperative mortality of 70-80% (in those cases without preoperative medical therapy). Patients, then, are considered to have a high risk of perioperative death once their mean PAP exceeds 35 mm_Hg.

Survival is best inferred from published institutional experiences. At one institution, without treatment, 1-year survival was 46% and 5-year survival was 14%. With medical therapy, 1-year survival was 88% and 5-year survival was 55%. Survival at 5 years with medical therapy followed by liver transplantation was 67%. At another institution, of the 67 patients with PPH from 1652 total cirrhotics evaluated for transplant, half (34) were placed on the waiting list. Of these, 16 (48%) were transplanted at a time when 25% of all patients who underwent full evaluation received new livers, meaning the diagnosis of PPH made a patient twice as likely to be transplanted, once on the waiting list. Of those listed for transplant with PPH, 11 (33%) were eventually removed because of PPH, and 5 (15%) died on the waitlist. Of the 16 transplanted patients with PPH, 11 (69%) survived for more than a year after transplant, at a time when overall one-year survival in that center was 86.4%. The three year post-transplant survival for patients with PPH was 62.5% when it was 81.02% overall at this institution.

Injury to the lung may also cause pulmonary edema through injury to the vasculature and parenchyma of the lung. The acute lung injury-acute respiratory distress syndrome (ALI-ARDS) covers many of these causes, but they may include:

- Inhalation of hot or toxic gases

- Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents)

- Aspiration, e.g., gastric fluid

- Reexpansion, i.e. post large volume thoracocentesis, resolution of pneumothorax, post decortication, removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema.

- Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation

- Swimming induced pulmonary edema also known as immersion pulmonary edema

- Transfusion Associated Circulatory Overload (TACO) occurs when multiple blood transfusions or blood-products (plasma, platelets, etc.) are transfused over a short period of time.

- Transfusion associated Acute Lung Injury (TRALI) is a specific type of blood-product transfusion injury that occurs when the donors plasma contained antibodies against the donor, such as anti-HLA or anti-neutrophil antibodies.

- Severe infection or inflammation which may be local or systemic. This is the classical form of ALI-ARDS.

Some causes of pulmonary edema are less well characterised and arguably represent specific instances of the broader classifications above.

- Arteriovenous malformation

- Hantavirus pulmonary syndrome

- High altitude pulmonary edema (HAPE)

- Envenomation, such as with the venom of Atrax robustus

Portopulmonary hypertension (PPH) is defined by the coexistence of portal and pulmonary hypertension. PPH is a serious complication of liver disease, present in 0.25 to 4% of all patients suffering from cirrhosis. Once an absolute contraindication to liver transplantation, it is no longer, thanks to rapid advances in the treatment of this condition. Today, PPH is comorbid in 4-6% of those referred for a liver transplant.

"Flash pulmonary edema" ("FPE"), is rapid onset pulmonary edema. It is most often precipitated by acute myocardial infarction or mitral regurgitation, but can be caused by aortic regurgitation, heart failure, or almost any cause of elevated left ventricular filling pressures. Treatment of FPE should be directed at the underlying cause, but the mainstays are ensuring adequate oxygenation, diuresis, and decrease of pulmonary circulation pressures.

Recurrence of FPE is thought to be associated with hypertension and may signify renal artery stenosis. Prevention of recurrence is based on managing hypertension, coronary artery disease, renovascular hypertension, and heart failure.

Smoking does not directly cause high blood pressure. However it is a known risk factor for other serious cardiovascular disease.

Pulmonary venoocclusive disease is rare, difficult to diagnose, and probably frequently misdiagnosed as idiopathic pulmonary arterial hypertension. Prevalence in parts of Europe is estimated to be 0.1-0.2 cases per million.

PVOD appears to occur as frequently in men as in women, and age at diagnosis ranges from 7–74 years with a median of 39 years. PVOD may occur in patients with associated diseases such as HIV, bone marrow transplantation, and connective tissue diseases. PVOD has also been associated with several chemotherapy regimens such as bleomycin, BCNU, and mitomycin.

The incidence of clinical HAPE in unacclimatized travelers exposed to high altitude (~) appears to be less than 1%. The U.S. Army Pike's Peak Research Laboratory has exposed sea-level-resident volunteers rapidly and directly to high altitude; during 30 years of research involving about 300 volunteers (and over 100 staff members), only three have been evacuated with suspected HAPE.

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.

Individual susceptibility to HAPE is difficult to predict. The most reliable risk factor is previous susceptibility to HAPE, and there is likely to be a genetic basis to this condition, perhaps involving the gene for angiotensin converting enzyme (ACE). Recently, scientists have found the similarities between low amounts of 2,3-BPG (also known as 2,3-DPG) with the occurrence of HAPE at high altitudes. Persons with sleep apnea are susceptible due to irregular breathing patterns while sleeping at high altitudes.

Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified as well as some rare genetic variants with large effects on blood pressure. Also, genome-wide association studies (GWAS) have identified 35 genetic loci related to blood pressure; 12 of these genetic loci influencing blood pressure were newly found. Sentinel SNP for each new genetic loci identified has shown an association with DNA methylation at multiple nearby Cpg sites. These sentinel SNP are located within genes related to vascular smooth muscle and renal function. DNA methylation might affect in some way linking common genetic variation to multiple phenotypes even though mechanisms underlying these associations are not understood. Single variant test performed in this study for the 35 sentinel SNP (known and new) showed that genetic variants singly or in aggregate contribute to risk of clinical phenotypes related to high blood pressure.

Blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable. Several environmental factors influence blood pressure. High salt intake raises the blood pressure in salt sensitive individuals; lack of exercise, obesity, and depression can play a role in individual cases. The possible role of other factors such as caffeine consumption, and vitamin D deficiency are less clear. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension. One review suggests that sugar may play an important role in hypertension and salt is just an innocent bystander.

Events in early life, such as low birth weight, maternal smoking, and lack of breastfeeding may be risk factors for adult essential hypertension, although the mechanisms linking these exposures to adult hypertension remain unclear. An increased rate of high blood urea has been found in untreated people with hypertensive in comparison with people with normal blood pressure, although it is uncertain whether the former plays a causal role or is subsidiary to poor kidney function. Average blood pressure may be higher in the winter than in the summer.

The symptoms for pulmonary veno-occlusive disease are the following:

This has a poor prognosis, as it is a fixed abnormality. Causes include post-term pregnancy, placental insufficiency, and NSAID use by the mother.

According to a recent study, the main risk factors for RA-ILD are advancing age, male sex, greater RA disease activity, rheumatoid factor (RF) positivity, and elevated titers of anticitrullinated protein antibodies such as anticyclic citrullinated peptide. Cigarette smoking also appears to increase risk of RA-ILD, especially in patients with human leukocyte antigen DRB1.

A recently published retrospective study by a team from Beijing Chao-Yang Hospital in Beijing, China, supported three of the risk factors listed for RA-ILD and identified an additional risk factor. In that study of 550 RA patients, logistic regression analysis of data collected on the 237 (43%) with ILD revealed that age, smoking, RF positivity, and elevated lactate dehydrogenase closely correlated with ILD.

Recent studies have identified risk factors for disease progression and mortality. A retrospective study of 167 patients with RA-ILD determined that the usual interstitial pneumonia (UIP) pattern on high-resolution computed tomography (HRCT) was a risk factor for progression, as were severe disease upon diagnosis and rate of change in pulmonary function test results in the first 6 months after diagnosis.

A study of 59 RA-ILD patients found no median survival difference between those with the UIP pattern and those without it. But the UIP group had more deaths, hospital admissions, need for supplemental oxygen, and decline in lung function.

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.

This has a good prognosis if it is reversible. Causes include polycythemia and hyperfibrinogenemia.

The exact cause of rheumatoid lung disease is unknown. However, associated factors could be due largely to smoking. Sometimes, the medicines used to treat rheumatoid arthritis, especially methotrexate, may result in lung disease.

Prevention's:

- Stop smoking: Chemicals found in cigarettes can irritate already delicate lung tissue, leading to further complications.

- Having regular checkups: The doctor could listen to lungs and monitor breathing, because lung problems that are detected early can be easier to treat.

In treating pulmonary insufficiency, it should be determined if pulmonary hypertension is causing the problem to therefore begin the most appropriate therapy as soon as possible (primary pulmonary hypertension or secondary pulmonary hypertension due to thromboembolism). Furthermore, pulmonary insufficiency is generally treated by addressing the underlying condition, in certain cases, the pulmonary valve may be surgically replaced.

Anomalous pulmonary venous connection (or anomalous pulmonary venous drainage or anomalous pulmonary venous return) is a congenital defect of the pulmonary veins.

Bilharzial cor pulmonale is the condition of right sided heart failure secondary to fibrosis and sclerosis of the pulmonary artery branches. It results from shifting of the "Schistosoma haematobium" ova from the pelvic and vescial plexus to the pulmonary artery branches where they settle and produce granuloma and fibrosis.

Bilharzial cor pulmonale occurs in "Schistosoma mansoni", when the portal pressure rises more than the systemic pressure. So blood will pass from the portal circulation to the systemic circulation carrying "Schistosoma mansoni" ova to reach the lungs.

This condition leads to Pulmonary hypertension, right ventricular hypertrophy and failure.

Prognosis of individuals with renovascular hypertension is not easy to determine. Those with atherosclerotic renal artery disease have a high risk of mortality, furthermore those who also have renal dysfunction have a higher mortality risk.

However, the majority of renovascular diseases can be improved with surgery.

Pulmonary diseases may also impact newborns, such as pulmonary hyperplasia, pulmonary interstitial emphysema (usually preterm births), and infant respiratory distress syndrome,