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.

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.

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.

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.

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

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.

Death may occur rapidly with acute, massive pulmonary bleeding or over longer periods as the result of continued pulmonary failure and right heart failure. Historically, patients had an average survival of 2.5 years after diagnosis, but today 86% may survive beyond five years.

Being idiopathic, IPH by definition has an unknown cause. It is thought to be an immune-mediated disease. The lung bleeding causes accumulation of iron, which in itself causes additional lung damage. Meanwhile, there is insufficient iron for inclusion into the haemoglobin molecules inside red blood cells which carry oxygen to body tissues for cellular respiration.

Idiopathic pulmonary haemosiderosis can occur either as a primary lung disorder or as the sequela to other pulmonary, cardiovascular or immune system disorder.

- PH1 involves PH with circulating anti-GBM antibodies.

- PH2 involves PH with immune complex disease such as systemic lupus erythematosus, SLE.

- PH3 involves no demonstrable immune system involvement.

A distinct subset of patients with pulmonary hemosiderosis has hypersensitivity to cow's milk which result in formation of IgG antibodies against basement membrane. This is called Heiner syndrome. Mechanism of haemorrhage is similar as in Goodpasture syndrome.

In the absence of severe urinary tract obstruction (which generally requires surgery with omental wrapping), treatment is generally with glucocorticoids initially, followed by DMARDs either as steroid-sparing agents or if refractory on steroids. The SERM tamoxifen has shown to improve the condition in various small trials, although the exact mechanism of its action remains unclear.

Associations include:

- Riedel's thyroiditis

- previous radiotherapy

- sarcoidosis

- inflammatory abdominal aortic aneurysm

- drugs

Perioperative PION patients have a higher prevalence of cardiovascular risk factors than in the general population. Documented cardiovascular risks in people affected by perioperative PION include high blood pressure, diabetes mellitus, high levels of cholesterol in the blood, tobacco use, abnormal heart rhythms, stroke, and obesity. Men are also noted to be at higher risk, which is in accordance with the trend, as men are at higher risk of cardiovascular disease. These cardiovascular risks all interfere with adequate blood flow, and also may suggest a contributory role of defective vascular autoregulation.

Causes of pulmonary hypoplasia include a wide variety of congenital malformations and other conditions in which pulmonary hypoplasia is a complication. These include congenital diaphragmatic hernia, congenital cystic adenomatoid malformation, fetal hydronephrosis, caudal regression syndrome, mediastinal tumor, and sacrococcygeal teratoma with a large component inside the fetus. Large masses of the neck (such as cervical teratoma) also can cause pulmonary hypoplasia, presumably by interfering with the fetus's ability to fill its lungs. In the presence of pulmonary hypoplasia, the EXIT procedure to rescue a baby with a neck mass is not likely to succeed.

Fetal hydrops can be a cause, or conversely a complication.

Pulmonary hypoplasia is associated with oligohydramnios through multiple mechanisms. Both conditions can result from blockage of the urinary bladder. Blockage prevents the bladder from emptying, and the bladder becomes very large and full. The large volume of the full bladder interferes with normal development of other organs, including the lungs. Pressure within the bladder becomes abnormally high, causing abnormal function in the kidneys hence abnormally high pressure in the vascular system entering the kidneys. This high pressure also interferes with normal development of other organs. An experiment in rabbits showed that PH also can be caused directly by oligohydramnios.

Pulmonary hypoplasia is associated with dextrocardia of embryonic arrest in that both conditions can result from early errors of development, resulting in Congenital cardiac disorders.

PH is a common direct cause of neonatal death resulting from pregnancy induced hypertension.

Management has three components: interventions before delivery, timing and place of delivery, and therapy after delivery.

In some cases, fetal therapy is available for the underlying condition; this may help to limit the severity of pulmonary hypoplasia. In exceptional cases, fetal therapy may include fetal surgery.

A 1992 case report of a baby with a sacrococcygeal teratoma (SCT) reported that the SCT had obstructed the outlet of the urinary bladder causing the bladder to rupture in utero and fill the baby's abdomen with urine (a form of ascites). The outcome was good. The baby had normal kidneys and lungs, leading the authors to conclude that obstruction occurred late in the pregnancy and to suggest that the rupture may have protected the baby from the usual complications of such an obstruction. Subsequent to this report, use of a vesicoamniotic shunting procedure (VASP) has been attempted, with limited success.

Often, a baby with a high risk of pulmonary hypoplasia will have a planned delivery in a specialty hospital such as (in the United States) a tertiary referral hospital with a level 3 neonatal intensive-care unit. The baby may require immediate advanced resuscitation and therapy.

Early delivery may be required in order to rescue the fetus from an underlying condition that is causing pulmonary hypoplasia. However, pulmonary hypoplasia increases the risks associated with preterm birth, because once delivered the baby requires adequate lung capacity to sustain life. The decision whether to deliver early includes a careful assessment of the extent to which delaying delivery may increase or decrease the pulmonary hypoplasia. It is a choice between expectant management and active management. An example is congenital cystic adenomatoid malformation with hydrops; impending heart failure may require a preterm delivery. Severe oligohydramnios of early onset and long duration, as can occur with early preterm rupture of membranes, can cause increasingly severe PH; if delivery is postponed by many weeks, PH can become so severe that it results in neonatal death.

After delivery, most affected babies will require supplemental oxygen. Some severely affected babies may be saved with extracorporeal membrane oxygenation (ECMO). Not all specialty hospitals have ECMO, and ECMO is considered the therapy of last resort for pulmonary insufficiency. An alternative to ECMO is high-frequency oscillatory ventilation.

The exact cause of lipodermatosclerosis is unknown. Venous disease, such as venous incompetence, venous hypertension, and body mass ("obesity") may be relevant to the underlying pathogenesis.

Increased blood pressure in the veins (venous hypertension) can cause diffusion of substances, including fibrin, out of capillaries. Fibrotic tissue may predispose the tissue to ulceration. Recurrent ulceration and fat necrosis is associated with lipodermatosclerosis. In advanced lipodermatosclerosis the proximal leg swells from chronic venous obstruction and the lower leg shrinks from chronic ulceration and fat necrosis resulting in the inverted coke bottle appearance of the lower leg.

Lipodermatosclerosis is most commonly diagnosed in middle-aged women.

The origin of lipodermatosclerosis is probably multifactorial, involving tissue hypoxia, leakage of proteins into the interstitium, and leukocyte activation. Studies of patients with lipodermatosclerosis have demonstrated significantly decreased concentrations of cutaneous oxygen associated with decreased capillary density. Capillaries are virtually absent in areas of fibrotic scars, leading to a condition known as atrophie blanche or livedoid vasculopathy.

Lipodermatosclerosis (also known as "chronic panniculitis with lipomembranous changes", "hypodermitis sclerodermiformis", "sclerosing panniculitis", and "stasis panniculitis") is a skin and connective tissue disease. It is a form of lower extremity panniculitis, an inflammation of the layer of fat under the epidermis.

As illustrated by the risk factors above, perioperative hypoxia is a multifactorial problem. Amidst these risk factors it may be difficult to pinpoint the optic nerve’s threshold for cell death, and the exact contribution of each factor.

Low blood pressure and anemia are cited as perioperative complications in nearly all reports of PION, which suggests a causal relationship. However, while low blood pressure and anemia are relatively common in the perioperative setting, PION is exceedingly rare. Spine and cardiac bypass surgeries have the highest estimated incidences of PION, 0.028% and 0.018% respectively, and this is still extremely low. This evidence suggests that optic nerve injury in PION patients is caused by more than just anemia and low blood pressure.

Evidence suggests that the multifactorial origin of perioperative PION involves the risks discussed above and perhaps other unknown factors. Current review articles of PION propose that vascular autoregulatory dysfunction and anatomic variation are under-investigated subjects that may contribute to patient-specific susceptibility.

Catamenial pneumothorax is a condition of air leaking into the pleural space (pneumothorax) occurring in conjunction with menstrual periods (catamenial refers to menstruation), believed to be caused primarily by endometriosis of the pleura (the membrane surrounding the lung).

Onset of lung collapse is less than 72 hours after menstruation. Typically, it occurs in women aged 30–40 years, but has been diagnosed in young girls as early as 10 years of age and post menopausal women (exclusively in women of menstrual age) most with a history of pelvic endometriosis.

Its association with various immune-related conditions and response to immunosuppression have led to speculation regarding an autoimmune cause of idiopathic RPF. One-third of the cases are secondary to malignancy, medication (methysergide, hydralazine, beta blockers), aortic aneurysm, or certain infections.

In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in "Pa"CO. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:

- Acute respiratory acidosis: HCO increases 1 mEq/L for each 10 mm Hg rise in "Pa"CO.

- Chronic respiratory acidosis: HCO rises 3.5 mEq/L for each 10 mm Hg rise in "Pa"CO.

The expected change in pH with respiratory acidosis can be estimated with the following equations:

- Acute respiratory acidosis: Change in pH = 0.008 X (40 − "Pa"CO)

- Chronic respiratory acidosis: Change in pH = 0.003 X (40 − "Pa"CO)

Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia.

Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragm function secondary to fatigue and hyperinflation.

Chronic respiratory acidosis also may be secondary to obesity hypoventilation syndrome (i.e., Pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial lung disease and thoracic deformities.

Lung diseases that primarily cause abnormality in alveolar gas exchange usually do not cause hypoventilation but tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue occurs.

Cortical necrosis is a severe and life-threatening condition, with mortality rates over 50%. Those mortality rates are even higher in neonates with the condition due to the overall difficult nature of neonatal care and an increased frequency of comorbid conditions. The extent of the necrosis is a major determinant of the prognosis, which in turn is dependent on the duration of ischemia, duration of oliguria, and the severity of the precipitating conditions. Of those that survive the initial event, there are varying degrees of recovery possible, depending on the extent of the damage.

There are two types of respiratory alkalosis: chronic and acute as a result of the 3-5 day delay in kidney compensation of the abnormality.

- "Acute respiratory alkalosis" occurs rapidly, have a high pH because the response of the kidneys is slow.

- "Chronic respiratory alkalosis" is a more long-standing condition, here one finds the kidneys have time to decrease the bicarbonate level.

Respiratory alkalosis is very rarely life-threatening, though pH level should not be 7.5 or greater. The aim in treatment is to detect the underlying cause. When PaCO2 is adjusted rapidly in individuals with chronic respiratory alkalosis, metabolic acidosis may occur. If the individual is on a mechanical ventilator then preventing hyperventilation is done via monitoring ABG levels.

Patients will require dialysis to compensate for the function of their kidneys.

Having cancer (current or previous) is currently one of the most prevalent out of all conditions among patients. High blood pressure, Chronic lung conditions, Alcohol abuse, Kidney failure, Malnutrition are another major risk factors.