Treatment of infants suffering birth asphyxia by lowering the core body temperature is now known to be an effective therapy to reduce mortality and improve neurological outcome in survivors, and hypothermia therapy for neonatal encephalopathy begun within 6 hours of birth significantly increases the chance of normal survival in affected infants.

There has long been a debate over whether newborn infants with birth asphyxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.

IH/BA is also a causitive factor in cardiac and circulatory birth defects the sixth most expensive condition, as well as premature birth and low birth weight the second most expensive and it is one of the contributing factors to infant respiratory distress syndrome (RDS) also known as hyaline membrane disease, the most expensive medical condition to treat and the number one cause of infant mortality.

Giving the mother glucocorticoids speeds the production of surfactant. For very premature deliveries, a glucocorticoid is given without testing the fetal lung maturity. The American College of Obstetricians and Gynecologists (ACOG), Royal College of Medicine, and other major organizations have recommended antenatal glucocorticoid treatment for women at risk for preterm delivery prior to 34 weeks of gestation. Multiple courses of glucocorticoid administration, compared with a single course, does not seem to increase or decrease the risk of death or neurodevelopmental disorders of the child.

In pregnancies of greater than 30 weeks, the fetal lung maturity may be tested by sampling the amount of surfactant in the amniotic fluid by amniocentesis, wherein a needle is inserted through the mother's abdomen and uterus. Several tests are available that correlate with the production of surfactant. These include the lecithin-sphingomyelin ratio ("L/S ratio"), the presence of phosphatidylglycerol (PG), and more recently, the surfactant/albumin (S/A) ratio. For the L/S ratio, if the result is less than 2:1, the fetal lungs may be surfactant deficient. The presence of PG usually indicates fetal lung maturity. For the S/A ratio, the result is given as mg of surfactant per gm of protein. An S/A ratio 55 indicates mature surfactant production(correlates with an L/S ratio of 2.2 or greater).

To counter the effects of high-altitude diseases, the body must return arterial p toward normal. Acclimatization, the means by which the body adapts to higher altitudes, only partially restores p to standard levels. Hyperventilation, the body’s most common response to high-altitude conditions, increases alveolar p by raising the depth and rate of breathing. However, while p does improve with hyperventilation, it does not return to normal. Studies of miners and astronomers working at 3000 meters and above show improved alveolar p with full acclimatization, yet the p level remains equal to or even below the threshold for continuous oxygen therapy for patients with chronic obstructive pulmonary disease (COPD). In addition, there are complications involved with acclimatization. Polycythemia, in which the body increases the number of red blood cells in circulation, thickens the blood, raising the danger that the heart can’t pump it.

In high-altitude conditions, only oxygen enrichment can counteract the effects of hypoxia. By increasing the concentration of oxygen in the air, the effects of lower barometric pressure are countered and the level of arterial p is restored toward normal capacity. A small amount of supplemental oxygen reduces the equivalent altitude in climate-controlled rooms. At 4000 m, raising the oxygen concentration level by 5 percent via an oxygen concentrator and an existing ventilation system provides an altitude equivalent of 3000 m, which is much more tolerable for the increasing number of low-landers who work in high altitude. In a study of astronomers working in Chile at 5050 m, oxygen concentrators increased the level of oxygen concentration by almost 30 percent (that is, from 21 percent to 27 percent). This resulted in increased worker productivity, less fatigue, and improved sleep.

Oxygen concentrators are uniquely suited for this purpose. They require little maintenance and electricity, provide a constant source of oxygen, and eliminate the expensive, and often dangerous, task of transporting oxygen cylinders to remote areas. Offices and housing already have climate-controlled rooms, in which temperature and humidity are kept at a constant level. Oxygen can be added to this system easily and relatively cheaply.

A prescription renewal for home oxygen following hospitalization requires an assessment of the patient for ongoing hypoxemia.

If the alveolar ventilation is insufficient, there will not be enough oxygen delivered to the alveoli for the body's use. This can cause hypoxemia even if the lungs are normal, as the cause is in the brainstem's control of ventilation or in the body's inability to breathe effectively.

Treatment of the underlying cause is required. Endotracheal intubation and mechanical ventilation are required in cases of severe respiratory failure (PaO2 less than 50 mmHg). Respiratory stimulants such as doxapram are rarely used, and if the respiratory failure resulted from an overdose of sedative drugs such as opioids or benzodiazepines, then the appropriate antidote (naloxone or flumazenil, respectively) will be given.

There is tentative evidence that in those with respiratory failure identified before arrival in hospital, continuous positive airway pressure can be useful when started before conveying to hospital.

"Hypoxemia" refers to low oxygen in the blood, and the more general term "hypoxia" is an abnormally low oxygen content in any tissue or organ, or the body as a whole. Hypoxemia can cause hypoxia (hypoxemic hypoxia), but hypoxia can also occur via other mechanisms, such as anemia.

Hypoxemia is usually defined in terms of reduced partial pressure of oxygen (mm Hg) in arterial blood, but also in terms of reduced content of oxygen (ml oxygen per dl blood) or percentage saturation of hemoglobin (the oxygen binding protein within red blood cells) with oxygen, which is either found singly or in combination.

While there is general agreement that an arterial blood gas measurement which shows that the partial pressure of oxygen is lower than normal constitutes hypoxemia, there is less agreement concerning whether the oxygen content of blood is relevant in determining hypoxemia. This definition would include oxygen carried by hemoglobin. The oxygen content of blood is thus sometimes viewed as a measure of tissue delivery rather than hypoxemia.

Just as extreme hypoxia can be called anoxia, extreme hypoxemia can be called anoxemia.

When the pulmonary capillary pressure remains elevated chronically (for at least 2 weeks), the lungs become even more resistant to pulmonary edema because the lymph vessels expand greatly, increasing their capability of carrying fluid away from the interstitial spaces perhaps as much as 10-fold. Therefore, in patients with chronic mitral stenosis, pulmonary capillary pressures of 40 to 45 mm Hg have been measured without the development of lethal pulmonary edema.[Guytun and Hall physiology]

Hypoxia exists when there is a reduced amount of oxygen in the tissues of the body. Hypoxemia refers to a reduction in PO2 below the normal range, regardless of whether gas exchange is impaired in the lung, CaO2 is adequate, or tissue hypoxia exists. There are several potential physiologic mechanisms for hypoxemia, but in patients with COPD the predominant one is V/Q mismatching, with or without alveolar hypoventilation, as indicated by PaCO2. Hypoxemia caused by V/Q mismatching as seen in COPD is relatively easy to correct, so that only comparatively small amounts of supplemental oxygen (less than 3 L/min for the majority of patients) are required for LTOT. Although hypoxemia normally stimulates ventilation and produces dyspnea, these phenomena and the other symptoms and signs of hypoxia are sufficiently variable in patients with COPD as to be of limited value in patient assessment. Chronic alveolar hypoxia is the main factor leading to development of cor pulmonale—right ventricular hypertrophy with or without overt right ventricular failure—in patients with COPD. Pulmonary hypertension adversely affects survival in COPD, to an extent that parallels the degree to which resting mean pulmonary artery pressure is elevated. Although the severity of airflow obstruction as measured by FEV1 is the best correlate with overall prognosis in patients with COPD, chronic hypoxemia increases mortality and morbidity for any severity of disease. Large-scale studies of LTOT in patients with COPD have demonstrated a dose-response relationship between daily hours of oxygen use and survival. There is reason to believe that continuous, 24-hours-per-day oxygen use in appropriately selected patients would produce a survival benefit even greater than that shown in the NOTT and MRC studies.

TTN is a diagnosis of exclusion as it is a benign condition that can have symptoms and signs similar to more serious conditions, such as respiratory distress syndrome. A chest X-ray may show a radiopaque line - fluid - in the horizontal fissure of the right lung, fluid infiltrate throughout alveoli or fluid in individual lung lobes. The lungs may also appear hyperinflated.

Transient tachypnea of the newborn occurs in approximately 1 in 100 preterm infants and 3.6-5.7 per 1000 term infants. It is most common in infants born by Cesarian section without a trial of labor after 35 weeks' gestation. Male infants and infants with an umbilical cord prolapse or perinatal asphyxia are at higher risk. Parental risk factors include use of pain control or anesthesia during labor, asthma, and diabetes.

The diagnosis is made by the clinical picture and the chest xray, which demonstrates decreased lung volumes (bell-shaped chest), absence of the thymus (after about 6 hours), a small (0.5–1 mm), discrete, uniform infiltrate (sometimes described as a "ground glass" appearance or as of recently described as "diffuse airspace and interstitial opacities") that involves all lobes of the lung, and air-bronchograms (i.e. the infiltrate will outline the larger airways passages which remain air-filled). In severe cases, this becomes exaggerated until the cardiac borders become inapparent (a 'white-out' appearance).

Respiratory failure results from inadequate gas exchange by the respiratory system, meaning that the arterial oxygen, carbon dioxide or both cannot be kept at normal levels. A drop in the oxygen carried in blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. Respiratory failure is classified as either Type I or Type II, based on whether there is a high carbon dioxide level. The definition of respiratory failure in clinical trials usually includes increased respiratory rate, abnormal blood gases (hypoxemia, hypercapnia, or both), and evidence of increased work of breathing.

The normal partial pressure reference values are: oxygen PaO more than , and carbon dioxide PaCO lesser than .

The rate of BPD varies among institutions, which may reflect neonatal risk factors, care practices (e.g., target levels for acceptable oxygen saturation), and differences in the clinical definitions of BPD.

The hepatopulmonary syndrome is suspected in any patient with known liver disease who reports dyspnea (particularly platypnea). Patients with clinically significant symptoms should undergo pulse oximetry. If the syndrome is advanced, arterial blood gasses should be measured on air.

A useful diagnostic test is contrast echocardiography. Intravenous microbubbles (> 10 micrometers in diameter) from agitated normal saline that are normally obstructed by pulmonary capillaries (normally <8 to 15 micrometers) rapidly transit the lung and appear in the left atrium of the heart within 7 heart beats. Similarly, intravenous technetium (99mTc) albumin aggregated may transit the lungs and appear in the kidney and brain. Pulmonary angiography may reveal diffusely fine or blotchy vascular configuration. The distinction has to be made with an intracardiac right-to-left shunt.

Let us consider some scenarios where there is a defect in ventilation and/ or perfusion of the lungs.

In condition such as pulmonary embolism, the pulmonary blood flow is affected, thus the ventilation of the lung is adequate, however there is a perfusion defect with defect in blood flow. Gas exchange thus becomes highly inefficient leading to hypoxemia as measured by arterial oxygenation. A ventilation perfusion scan or lung scintigraphy shows some areas of lungs being ventilated but not adequately perfused. This also leads to a high A-a gradient which is not responsive to oxygen

In conditions with right to left shunts, there is again a ventilation perfusion defect with high A-a gradient. However, the A-a gradient is responsive to oxygen therapy. In cases of right to left shunts more of deoxygenated blood mixes with oxygenated blood from the lungs and thus to a small extent the condition might neutralize the high A-a gradient with pure oxygen therapy.

Patient with parenchymal lung diseases will have an increased A-a gradient with moderate response to oxygen therapy.

A patient with hypoventilation will have complete response to 100% oxygen therapy

The following tests have been promoted as supposedly diagnosing placental insufficiency, but all have been unsuccessful at predicting stillbirth due to placental insufficiency:

- Placental grading

- Amniotic fluid index

- Fetal biophysical profile test scoring

- Doppler velocimetry

- Routine ultrasound scanning

- Detection and management of maternal diabetes mellitus

- Antenatal fetal heart rate monitoring using cardiotocography

- Vibroacoustic stimulation, fetal movement counting

- Home vs. hospital-based bed rest and monitoring in high-risk pregnancy

- In-hospital fetal surveillance unit

- Use of the partograph during labor

- Cardiotocography during labor with or without pulse oximetry

The classic diagnosis of BPD may be assigned at 28 days of life if the following criteria are met:

1. Positive pressure ventilation during the first 2 weeks of life for a minimum of 3 days.

2. Clinical signs of abnormal respiratory function.

3. Requirements for supplemental oxygen for longer than 28 days of age to maintain PaO2 above 50 mm Hg.

4. Chest radiograph with diffuse abnormal findings characteristic of BPD.

With liver transplantation, the 5 year survival rate is 74%, which is comparable to patients who undergo liver transplants who do not suffer from hepatopulmonary syndrome.

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

A 2008 bulletin from the World Health Organization estimates that 900,000 total infants die each year from birth asphyxia, making it a leading cause of death for newborns.

In the United States, intrauterine hypoxia and birth asphyxia was listed as the tenth leading cause of neonatal death.

Treatment aims to increase the amount of oxygen in the blood and reverse any causes of hypoxia.

- oxygen therapy

- mechanical ventilation

- Nitrous Oxide (NO·) Inhalation

- Prostaglandins (intravenous)

The therapies available to manage PPHN include the high frequency ventilation, surfactant instillation, inhaled nitric oxide, and extracorporeal membrane oxygenation. These expensive and/or invasive modalities are unavailable in the developing countries where the frequency and mortality of PPHN is likely to be much higher due to higher incidence of asphyxia and sepsis. In developing countries, the medical facilities are usually supplied with outdated equipment that was initially donated. "For people in developing countries, basic medical supplies are luxuries that are simply not available or not affordable. Doctors and nurses must constantly make do - washing and reusing "disposable" gloves and syringes, or substituting inappropriate materials such as fishing line or sewing thread for suture- or patients must go without needed care. In many countries patients must bring their own supplies, even acquire their own medicines, before treatment can be given." The limitations made it necessary to search for cheaper therapies, assuring quick effectiveness and stabilization of the patient going through a very high-risk situation. The treatments are chosen on the basis of low cost, low-tech, wide availability, and safety in the hands of non-professionals. Therefore, oral sildenafil citrate, has been the alternative way of therapy. The cost comparison shows that sildenafil is lower in cost than iNO and more readily available. There is improvement in oxygenation when oral sildenifal is administered according to the studies found in the Official Journal of the American Academy of Pediatric. The positive research results for varies studies indicates that oral sildenifal is a feasible source to improve oxygenation and survival in critical ill infants with PPHN secondary to parenchymal lung disease in centers without access to high-frequency ventilation, iNO, or ECMO.

There are 3 possible ways to test the fetal antigen status. Free Cell DNA, Amniocentesis, and Chorionic Villus Sampling. Of the three, CVS is no longer used due to risk of worsening the maternal antibody response. Once antigen status has been determined, assessment may be done with MCA scans.

- Free Cell DNA can be run on certain antigens. Blood is taken from the mother, and using PCR, can detect the K, C, c, D, and E alleles of fetal DNA. This blood test is non-invasive to the fetus and is an easy way of checking antigen status and risk of HDN. Testing has proven very accurate and is routinely done in the UK at the International Blood Group Reference Laboratory in Bristol. Sanequin laboratory in Amsterdam, Netherlands also performs this test. For US patients, blood may be sent to either of the labs. In the US, Sensigene is done by Sequenome to determine fetal D status. Sequenome does not accept insurance in the US, but US and Canadian patients have had insurance cover the testing done overseas.

- Amniocentesis is another recommended method for testing antigen status and risk for HDN. Fetal antigen status can be tested as early as 15 weeks by PCR of fetal cells.

- CVS is possible as well to test fetal antigen status but is not recommended. CVS carries a higher risk of fetal maternal hemorrhage and can raise antibody titers, potentially worsening the antibody effect.

There are several intervention options available in early, mid and late pregnancies.

Ventilation Perfusion mismatch or "V/Q defects" are defects in total lung ventilation perfusion ratio. It is a condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen due to some diseases and disorders.

The V/Q ratio of a healthy lung is approximately equal to 0.8, as normal lungs are not perfectly matched., which means the rate of alveolar ventilation to the rate of pulmonary blood flow is roughly equal.

The ventilation perfusion ratio can be measured by measuring the A-a gradient i.e. the alveolar-arterial gradient.

There is current controversy regarding the medicolegal definitions and impacts of birth asphyxia. Plaintiff's attorneys often take the position that birth asphyxia is often preventable, and is often due to substandard care and human error. They have utilized some studies in their favor that have demonstrated that, "...although other potential causes exist, asphyxia and hypoxic-ischemic encephalopathy affect a substantial number of babies, and they are preventable causes of cerebral palsy." The American Congress of Obstetricians and Gynecologists disputes that conditions such as cerebral palsy are usually attributable to preventable causes, instead associating them with circumstances arising prior to birth and delivery.