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In those with underlying heart disease, effective control of congestive symptoms prevents pulmonary edema.
Dexamethasone is in widespread use for the prevention of high altitude pulmonary edema. Sildenafil is used as a preventive treatment for altitude-induced pulmonary edema and pulmonary hypertension, the mechanism of action is via phosphodiesterase inhibition which raises cGMP, resulting in pulmonary arterial vasodilation and inhibition of smooth muscle cell proliferation. While this effect has only recently been discovered, sildenafil is already becoming an accepted treatment for this condition, in particular in situations where the standard treatment of rapid descent has been delayed for some reason.
The initial management of pulmonary edema, irrespective of the type or cause, is supporting vital functions. Therefore, if the level of consciousness is decreased it may be required to proceed to tracheal intubation and mechanical ventilation to prevent airway compromise. Hypoxia (abnormally low oxygen levels) may require supplementary oxygen, but if this is insufficient then again mechanical ventilation may be required to prevent complications. Treatment of the underlying cause is the next priority; pulmonary edema secondary to infection, for instance, would require the administration of appropriate antibiotics.
The dual (ET and ET) endothelin receptor antagonist bosentan was approved in 2001. Sitaxentan (Thelin) was approved for use in Canada, Australia, and the European Union, but not in the United States. In 2010, Pfizer withdrew Thelin worldwide because of fatal liver complications. A similar drug, ambrisentan is marketed as Letairis in the U.S. by Gilead Sciences.
Cyanosis is defined as the bluish or purplish discolouration of the skin or mucous membranes due to the tissues near the skin surface having low oxygen saturation. Based on Lundsgaard and Van Slyke's work, it is classically described as occurring if 5.0 g/dL of deoxyhemoglobin or greater is present. This was based on an estimate of capillary saturation based on a mean of arterial versus peripheral venous blood gas measurements. Since estimation of hypoxia is usually now based either on arterial blood gas measurement or pulse oximetry, this is probably an overestimate, with evidence that levels of 2.0 g/dL of deoxyhemoglobin may reliably produce cyanosis. Since, however, the presence of cyanosis is dependent upon there being an absolute quantity of deoxyhemoglobin, the bluish color is more readily apparent in those with high hemoglobin counts than it is with those with anemia. Also, the bluer the color, the more difficult it is to detect on deeply pigmented skin. When signs of cyanosis first appear, such as on the lips or fingers, intervention should be made within 3–5 minutes because a severe hypoxia or severe circulatory failure may have induced the cyanosis.
The name "cyanosis" literally means "the blue disease" or "the blue condition". It is derived from the color cyan, which comes from κυανός, "kyanós", the Greek word for "blue".
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.
To help understand factors that make some individuals susceptible to HAPE, the International HAPE Database was set up in 2004. The database is administered by APEX, a high altitude medical research charity. Individuals who have previously suffered from HAPE can register with this confidential database to help researchers study the condition.
Differential cyanosis is the bluish coloration of the lower but not the upper extremity and the head. This is seen in patients with a patent ductus arteriosus. Patients with a large ductus develop progressive pulmonary vascular disease, and pressure overload of the right ventricle occurs. As soon as pulmonary pressure exceeds aortic pressure, shunt reversal (right-to-left shunt) occurs. The upper extremity remains pink because the brachiocephalic trunk, left common carotid trunk and the left subclavian trunk is given off proximal to the PDA.
The U.S. FDA approved sildenafil, a selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5), for the treatment of PAH in 2005. It is marketed for PAH as Revatio. In 2009, they also approved tadalafil, another PDE5 inhibitor, marketed under the name Adcirca. PDE5 inhibitors are believed to increase pulmonary artery vasodilation, and inhibit vascular remodeling, thus lowering pulmonary arterial pressure and pulmonary vascular resistance.
Tadalafil is taken orally, as well as sildenafil, and it is rapidly absorbed (serum levels are detectable at 20 minutes). The T (biological half-life) hovers around 17.5 hours in healthy subjects. Moreover, if we consider pharmacoeconomic implications, patients that take tadalafil would pay two-thirds of the cost of sildenafil therapy. However, there are some adverse effects of this drug such as headache, diarrhea, nausea, back pain, dyspepsia, flushing and myalgia.
The term hypoxemia was originally used to describe low blood oxygen occurring at high altitudes and was defined generally as defective oxygenation of the blood.
Treatment is directed at correcting the underlying cause. Post-surgical atelectasis is treated by physiotherapy, focusing on deep breathing and encouraging coughing. An incentive spirometer is often used as part of the breathing exercises. Walking is also highly encouraged to improve lung inflation. People with chest deformities or neurologic conditions that cause shallow breathing for long periods may benefit from mechanical devices that assist their breathing. One method is continuous positive airway pressure, which delivers pressurized air or oxygen through a nose or face mask to help ensure that the alveoli do not collapse, even at the end of a breath. This is helpful, as partially inflated alveoli can be expanded more easily than collapsed alveoli. Sometimes additional respiratory support is needed with a mechanical ventilator.
The primary treatment for acute massive atelectasis is correction of the underlying cause. A blockage that cannot be removed by coughing or by suctioning the airways often can be removed by bronchoscopy. Antibiotics are given for an infection. Chronic atelectasis is often treated with antibiotics because infection is almost inevitable. In certain cases, the affected part of the lung may be surgically removed when recurring or chronic infections become disabling or bleeding is significant. If a tumor is blocking the airway, relieving the obstruction by surgery, radiation therapy, chemotherapy, or laser therapy may prevent atelectasis from progressing and recurrent obstructive pneumonia from developing.
In conditions where the proportion of oxygen in the air is low, or when the partial pressure of oxygen has decreased, less oxygen is present in the alveoli of the lungs. The alveolar oxygen is transferred to hemoglobin, a carrier protein inside red blood cells, with an efficiency that decreases with the partial pressure of oxygen in the air.
- Altitude. The external partial pressure of oxygen decreases with altitude, for example in areas of high altitude or when flying. This decrease results in decreased carriage of oxygen by haemoglobin. This is particularly seen as a cause of cerebral hypoxia and mountain sickness in climbers of Mount Everest and other peaks of extreme altitude. For example, at the peak of Mount Everest, the partial pressure of oxygen is just 43 mmHg, whereas at sea level the partial pressure is 150 mmHg. For this reason, cabin pressure in aircraft is maintained at 5,000 to 6,000 feet (1500 to 1800 m).
- Diving. Hypoxia in diving can result from sudden surfacing. The partial pressures of gases increases when diving, increases by one ATM every ten metres. This means that a partial pressure of oxygen sufficient to maintain good carriage by haemoglobin is possible at depth, even if it is insufficient at the surface. A diver that remains underwater will slowly consume their oxygen, and when surfacing, the partial pressure of oxygen may be insufficient (shallow water blackout). This may manifest at depth as deep water blackout.
- Suffocation. Decreased concentration of oxygen in inspired air caused by reduced replacement of oxygen in the breathing mix.
- Anaesthetics. Low partial pressure of oxygen in the lungs when switching from inhaled anesthesia to atmospheric air, due to the Fink effect, or diffusion hypoxia.
- Air depleted of oxygen has also proven fatal. In the past, anesthesia machines have malfunctioned, delivering low-oxygen gas mixtures to patients. Additionally, oxygen in a confined space can be consumed if carbon dioxide scrubbers are used without sufficient attention to supplementing the oxygen which has been consumed.
Pulmonary embolism may be preventable in those with risk factors. People admitted to hospital may receive preventative medication, including unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux, and anti-thrombosis stockings to reduce the risk of a DVT in the leg that could dislodge and migrate to the lungs.
Following the completion of warfarin in those with prior PE, long-term aspirin is useful to prevent recurrence.
Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently, it has gone through a resurgence with the revision of the surgical technique and is thought to benefit certain people. Chronic pulmonary embolism leading to pulmonary hypertension (known as "chronic thromboembolic hypertension") is treated with a surgical procedure known as a pulmonary thromboendarterectomy.
Along with the measure above, systemic immediate release opioids are beneficial in emergently reducing the symptom of shortness of breath due to both cancer and non cancer causes; long-acting/sustained-release opioids are also used to prevent/continue treatment of dyspnea in palliative setting. Pulmonary rehabilitation may alleviate symptoms in some people, such as those with COPD, but will not cure the underlying disease. There is a lack of evidence to recommend midazolam, nebulised opioids, the use of gas mixtures, or cognitive-behavioral therapy.
In those who are not palliative the primary treatment of shortness of breath is directed at its underlying cause. Extra oxygen is effective in those with hypoxia; however, this has no effect in those with normal blood oxygen saturations, even in those who are palliative.
The most common cause is post-surgical atelectasis, characterized by splinting, i.e. restricted breathing after abdominal surgery.
Another common cause is pulmonary tuberculosis. Smokers and the elderly are also at an increased risk. Outside of this context, atelectasis implies some blockage of a bronchiole or bronchus, which can be within the airway (foreign body, mucus plug), from the wall (tumor, usually squamous cell carcinoma) or compressing from the outside (tumor, lymph node, tubercle). Another cause is poor surfactant spreading during inspiration, causing the surface tension to be at its highest which tends to collapse smaller alveoli. Atelectasis may also occur during suction, as along with sputum, air is withdrawn from the lungs. There are several types of atelectasis according to their underlying mechanisms or the distribution of alveolar collapse; resorption, compression, microatelectasis and contraction atelectasis.
The administration of fluid therapy in individuals with pulmonary contusion is controversial. Excessive fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage from injured capillaries (pulmonary edema), which are more permeable than normal. However, low blood volume (hypovolemia) resulting from insufficient fluid has an even worse impact, potentially causing hypovolemic shock; for people who have lost large amounts of blood, fluid resuscitation is necessary. A lot of the evidence supporting the idea that fluids should be withheld from people with pulmonary contusion came from animal studies, not clinical trials with humans; human studies have had conflicting findings on whether fluid resuscitation worsens the condition. Current recommendations suggest giving enough fluid to ensure sufficient blood flow but not giving any more fluid than necessary. For people who do require large amounts of intravenous fluid, a catheter may be placed in the pulmonary artery to measure the pressure within it. Measuring pulmonary artery pressure allows the clinician to give enough fluids to prevent shock without exacerbating edema. Diuretics, drugs that increase urine output to reduce excessive fluid in the system, can be used when fluid overload does occur, as long as there is not a significant risk of shock. Furosemide, a diuretic used in the treatment of pulmonary contusion, also relaxes the smooth muscle in the veins of the lungs, thereby decreasing pulmonary venous resistance and reducing the pressure in the pulmonary capillaries.
Positive pressure ventilation, in which air is forced into the lungs, is needed when oxygenation is significantly impaired. Noninvasive positive pressure ventilation including continuous positive airway pressure (CPAP) and bi-level positive airway pressure (BiPAP), may be used to improve oxygenation and treat atelectasis: air is blown into the airways at a prescribed pressure via a face mask. Noninvasive ventilation has advantages over invasive methods because it does not carry the risk of infection that intubation does, and it allows normal coughing, swallowing, and speech. However, the technique may cause complications; it may force air into the stomach or cause aspiration of stomach contents, especially when level of consciousness is decreased.
People with signs of inadequate respiration or oxygenation may need to be intubated and mechanically ventilated. Mechanical ventilation aims to reduce pulmonary edema and increase oxygenation. Ventilation can reopen collapsed alveoli, but it is harmful for them to be repeatedly opened, and positive pressure ventilation can also damage the lung by overinflating it. Intubation is normally reserved for when respiratory problems occur, but most significant contusions do require intubation, and it may be done early in anticipation of this need. People with pulmonary contusion who are especially likely to need ventilation include those with prior severe lung disease or kidney problems; the elderly; those with a lowered level of consciousness; those with low blood oxygen or high carbon dioxide levels; and those who will undergo operations with anesthesia. Larger contusions have been correlated with a need for ventilation for longer periods of time.
Pulmonary contusion or its complications such as acute respiratory distress syndrome may cause lungs to lose compliance (stiffen), so higher pressures may be needed to give normal amounts of air and oxygenate the blood adequately. Positive end-expiratory pressure (PEEP), which delivers air at a given pressure at the end of the expiratory cycle, can reduce edema and keep alveoli from collapsing. PEEP is considered necessary with mechanical ventilation; however, if the pressure is too great it can expand the size of the contusion and injure the lung. When the compliance of the injured lung differs significantly from that of the uninjured one, the lungs can be ventilated independently with two ventilators in order to deliver air at different pressures; this helps avoid injury from overinflation while providing adequate ventilation.
MAS is difficult to prevent. Amnioinfusion, a method of thinning thick meconium that has passed into the amniotic fluid through pumping of sterile fluid into the amniotic fluid, has not shown a benefit.
The mortality rate of meconium-stained infants is considerably higher than that of non-stained infants; meconium aspiration used to account for a significant proportion of neonatal deaths. Residual lung problems are rare but include symptomatic cough, wheezing, and persistent hyperinflation for up to five to ten years. The ultimate prognosis depends on the extent of CNS injury from asphyxia and the presence of associated problems such as pulmonary hypertension. Fifty percent of newborns affected by meconium aspiration would die fifteen years ago; however, today the percent has dropped to about twenty.
The risk may be reduced by administering a non-particulate antacid (e.g. Sodium Citrate) or an H-antagonist like Ranitidine.
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.
It is sometimes treated with surgery, which involves rerouting blood from the right atrium into the left atrium with a patch or use of the Warden procedure. However, interest is increasing in catheter-based interventional approaches, as well as medical therapy for less severe cases.
A preventative procedure (thoracotomy or thoracoscopy with pleurodesis) may be recommended after an episode of pneumothorax, with the intention to prevent recurrence. Evidence on the most effective treatment is still conflicting in some areas, and there is variation between treatments available in Europe and the US. Not all episodes of pneumothorax require such interventions; the decision depends largely on estimation of the risk of recurrence. These procedures are often recommended after the occurrence of a second pneumothorax. Surgery may need to be considered if someone has experienced pneumothorax on both sides ("bilateral"), sequential episodes that involve both sides, or if an episode was associated with pregnancy.
If pneumothorax occurs in a smoker, this is considered an opportunity to emphasize the markedly increased risk of recurrence in those who continue to smoke, and the many benefits of smoking cessation. It may be advisable for someone to remain off work for up to a week after a spontaneous pneumothorax. If the person normally performs heavy manual labor, several weeks may be required. Those who have undergone pleurodesis may need two to three weeks off work to recover.
Air travel is discouraged for up to seven days after complete resolution of a pneumothorax if recurrence does not occur. Underwater diving is considered unsafe after an episode of pneumothorax unless a preventative procedure has been performed. Professional guidelines suggest that pleurectomy be performed on both lungs and that lung function tests and CT scan normalize before diving is resumed. Aircraft pilots may also require assessment for surgery.