Pulmonary edema

Last updated
Pulmonary edema
Other namesPulmonary oedema
PulmEdema.PNG
Pulmonary edema with small pleural effusions on both sides
Specialty Cardiology, critical care medicine pulmonology
Symptoms Progressive dyspnea, cough, fever, cyanosis, tachycardia
Complications ARDS, respiratory failure
CausesCardiogenic, Noncardiogenic (pneumonia, inhalation injury, sepsis, airway obstruction, high altitude)
Diagnostic method Medical imaging, lab tests, ECG, echocardiography
TreatmentSupplemental oxygen, diuretics, treat underlying disease process

Pulmonary edema (British English: oedema), also known as pulmonary congestion, is excessive fluid accumulation in the tissue or air spaces (usually alveoli) of the lungs. [1] This leads to impaired gas exchange, most often leading to dyspnea which can progress to hypoxemia and respiratory failure. Pulmonary edema has multiple causes and is traditionally classified as cardiogenic (caused by the heart) or noncardiogenic (all other types not caused by the heart). [2] [3]

Contents

Various laboratory tests (CBC, troponin, BNP, etc.) and imaging studies (chest x-ray, CT scan, ultrasound) are often used to diagnose and classify the cause of pulmonary edema. [4] [5] [6] Treatment is focused on three aspects: improving respiratory function, treating the underlying cause, and preventing further damage and allow full recovery to the lung. Pulmonary edema can cause permanent organ damage, and when sudden (acute), can lead to respiratory failure or cardiac arrest due to hypoxia. [7] The term edema is from the Greek οἴδημα (oidēma, "swelling"), from οἰδέω (oidéō, "(I) swell"). [8] [9]

Pathophysiology

The amount of fluid in the lungs is governed by multiple forces and is visualized using the Starling equation. There are two hydrostatic pressures and two oncotic (protein) pressures that determine the fluid movement within the lung air spaces (alveoli). Of the forces that explain fluid movement, only the pulmonary wedge pressure is obtainable via pulmonary artery catheterization. [10] Due to the complication rate associated with pulmonary artery catheterization, other imaging modalities and diagnostic methods have become more popular. [11] Imbalance in any of these forces can cause fluid movement (or lack of movement) causing a buildup of fluid where it should not normally be. Although rarely clinically measured, these forces allow us to classify, and subsequently treat the underlying cause of pulmonary edema.

Classification

Pulmonary edema has a multitude of causes, and is typically classified as cardiogenic or noncardiogenic. Cardiogenic pulmonary edema is caused by increased hydrostatic pressure causing increased fluid in the pulmonary interstitium and alveoli. Noncardiogenic causes are associated with the oncotic pressure as discussed above causing malfunctioning barriers in the lungs (increased microvascular permeability). [12]

Cardiogenic

Cardiogenic pulmonary edema is typically caused by either volume overload or impaired left ventricular function. As a result, pulmonary pressures rises from the normal average of 15 mmHg. [13] As the pulmonary pressure rises, these pressures overwhelm the barriers and fluid enters the alveoli when the pressure is above 25 mmHg. [14] Depending whether the cause is acute or chronic determines how fast pulmonary edema develops and the severity of symptoms. [12] Some of the common causes of cardiogenic pulmonary edema include:

Flash Pulmonary Edema

A particularly severe type of cardiogenic pulmonary edema is flash pulmonary edema (FPE). Flash pulmonary edema is a clinical syndrome of acute heart failure that begins suddenly and accelerates rapidly. Frequently the most noticeable abnormality is edema of the lungs. Nevertheless it is a cardiovascular disease not a pulmonary disease. It is also known by other appellations including sympathetic crashing acute pulmonary edema (SCAPE). [18] It is often associated with severe hypertension [19] Typically, patients with the syndrome of flash pulmonary edema do not have chest pain.  Treatment of FPE should include reducing systemic vascular resistance with nitroglycerin, ensuring adequate oxygenation with non-invasive ventilation, and decrease of pulmonary circulation pressures while FPE stays. [20]

Recurrence of FPE is thought to be associated with hypertension [21] and may signify renal artery stenosis. [22] Prevention of recurrence is based on managing or preventing hypertension, coronary artery disease, renovascular hypertension, and heart failure.

Noncardiogenic

Noncardiogenic pulmonary edema is caused by increased microvascular permeability (increased oncotic pressure) leading to increased fluid transfer into the alveolar spaces. The pulmonary artery wedge pressure is typically normal as opposed to cardiogenic pulmonary edema where the elevated pressure is causing the fluid transfer. There are multiple causes of noncardiogenic edema with multiple subtypes within each cause. Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Although ARDS can present with pulmonary edema (fluid accumulation), it is a distinct clinical syndrome that is not synonymous with pulmonary edema.

Direct Lung Injury

Acute lung injury may cause pulmonary edema directly through injury to the vasculature and parenchyma of the lung, causes include:

Indirect Lung Injury

Special Causes

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

Signs and symptoms

Fluid within the alveoli (air spaces) of the lungs Respiratory system - Pulmonary edema -- Smart-Servier.png
Fluid within the alveoli (air spaces) of the lungs

The most common symptom of pulmonary edema is dyspnea and may include other symptoms relating to inadequate oxygen (hypoxia) such as fast breathing (tachypnea), tachycardia and cyanosis. Other common symptoms include coughing up blood (classically seen as pink or red, frothy sputum), excessive sweating, anxiety, and pale skin. Other signs include end-inspiratory crackles (crackling sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound. [3]

Shortness of breath can manifest as orthopnea (inability to breathe sufficiently when lying down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic and cardiogenic pulmonary edema due to left ventricular failure.

The development of pulmonary edema may be associated with symptoms and signs of "fluid overload" in the lungs; this is a non-specific term to describe the manifestations of right ventricular failure on the rest of the body. These symptoms may include peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon due to fluid), raised jugular venous pressure and hepatomegaly, where the liver is excessively enlarged and may be tender or even pulsatile.

Additional symptoms such as fever, low blood pressure, injuries or burns may be present and can help characterize the cause and subsequent treatment strategies.

Diagnosis

Chest X-ray of Pulmonary Edema with lines and overlay showing congestion Comparison PE.png
Chest X-ray of Pulmonary Edema with lines and overlay showing congestion

There is no single test for confirming that breathlessness is caused by pulmonary edema – there are many causes of shortness of breath; but there are methods to suggest a high probability of an edema.

Lab Tests

Low oxygen saturation in blood and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Elevated creatine levels may suggest a cardiogenic cause of pulmonary edema. [12] Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT) are also typically requested as further diagnosis. Elevated white blood cell count (WBC) may suggest a non-cardiogenic cause such as sepsis or infection. [12] B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) suggest a cardiac cause is unlikely, and suggest noncardiogenic pulmonary edema. [3]

Imaging Tests

Pulmonary edema on CT-scan (coronal MPR) 18-01-Lungenoedem CT coronar.png
Pulmonary edema on CT-scan (coronal MPR)

Chest X-ray has been used for many years to diagnose pulmonary edema due to its wide availability and relatively cheap cost. [4] A chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (biased blood flow to the superior parts instead of inferior parts of the lung), and possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edema. [3]

Lung ultrasounds, employed by a healthcare provider at the point of care, is also a useful tool to diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water, track changes over time, and differentiate between cardiogenic and non-cardiogenic edema. [36] Lung ultrasound is recommended as the first-line method due to its wide availability, ability to be performed bedside, and wide diagnostic utility for other similar diseases. [4]

Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous pressures and high pulmonary artery pressures leading to pulmonary edema.

Prevention

In those with underlying heart or lung disease, effective control of congestive and respiratory symptoms can help prevent pulmonary edema. [37]

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. [38] [39] Sildenafil's mechanism of action is via phosphodiesterase inhibition which raises cGMP, resulting in pulmonary arterial vasodilation and inhibition of smooth muscle cell proliferation and indirectly fluid formation in the lungs. [40] 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 (acclimatization) has been delayed for some reason. [41]

Management

The initial management of pulmonary edema, irrespective of the type or cause, is supporting vital functions while edema lasts. Hypoxia may require supplementary oxygen to balance blood oxygen levels, but if this is insufficient then again mechanical ventilation may be required to prevent complications caused by hypoxia. [42] Therefore, if the level of consciousness is decreased it may be required to proceed to tracheal intubation and mechanical ventilation to prevent airway compromise. Treatment of the underlying cause is the next priority; pulmonary edema secondary to infection, for instance, would require the administration of appropriate antibiotics or antivirals. [2] [3]

Cardiogenic pulmonary edema

Acute cardiogenic pulmonary edema often responds rapidly to medical treatment. [43] Positioning upright may relieve symptoms. A loop diuretic such as furosemide (or Lasix®) is administered, often together with morphine to reduce respiratory distress. [43] Both diuretic and morphine may have vasodilator effects, but specific vasodilators may be used (particularly intravenous glyceryl trinitrate or ISDN) provided the blood pressure is adequate. [43]

Continuous positive airway pressure and bilevel positive airway pressure (CPAP/BiPAP) has been demonstrated to reduce mortality and the need of mechanical ventilation in people with severe cardiogenic pulmonary edema. [44]

It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock, in which the cardiac output is insufficient to sustain an adequate blood pressure to the lungs. This can be treated with inotropic agents or by intra-aortic balloon pump, but this is regarded as temporary treatment while the underlying cause is addressed and the lungs recover. [43]

Prognosis

As pulmonary edema has a wide variety of causes and presentations, the outcome or prognosis is often disease-dependent and more accurately described in relation to the associated syndrome. It is a major health problem, with one large review stating an incidence of 7.6% with an associated in hospital mortality rate of 11.9%. [2] Generally, pulmonary edema is associated with a poor prognosis with a 50% survival rate at one year, and 85% mortality at six years. [45]

Related Research Articles

<span class="mw-page-title-main">Hypoxia (medicine)</span> Medical condition of lack of oxygen in the tissues

Hypoxia is a condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level. Hypoxia may be classified as either generalized, affecting the whole body, or local, affecting a region of the body. Although hypoxia is often a pathological condition, variations in arterial oxygen concentrations can be part of the normal physiology, for example, during strenuous physical exercise.

<span class="mw-page-title-main">Edema</span> Accumulation of excess fluid in body tissue

Edema, also spelled oedema, and also known as fluid retention, dropsy, hydropsy and swelling, is the build-up of fluid in the body's tissue. Most commonly, the legs or arms are affected. Symptoms may include skin which feels tight, the area may feel heavy, and joint stiffness. Other symptoms depend on the underlying cause.

<span class="mw-page-title-main">Respiratory failure</span> Inadequate gas exchange by the respiratory system

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 the blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. Respiratory failure is classified as either Type 1 or Type 2, based on whether there is a high carbon dioxide level, and can be acute or chronic. In clinical trials, the definition of respiratory failure usually includes increased respiratory rate, abnormal blood gases, and evidence of increased work of breathing. Respiratory failure causes an altered mental status due to ischemia in the brain.

<span class="mw-page-title-main">Obesity hypoventilation syndrome</span> Condition in which severely overweight people fail to breathe rapidly or deeply enough

Obesity hypoventilation syndrome (OHS) is a condition in which severely overweight people fail to breathe rapidly or deeply enough, resulting in low oxygen levels and high blood carbon dioxide (CO2) levels. The syndrome is often associated with obstructive sleep apnea (OSA), which causes periods of absent or reduced breathing in sleep, resulting in many partial awakenings during the night and sleepiness during the day. The disease puts strain on the heart, which may lead to heart failure and leg swelling.

<span class="mw-page-title-main">Pulmonary heart disease</span> Medical condition

Pulmonary heart disease, also known as cor pulmonale, is the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs.

<span class="mw-page-title-main">Acute respiratory distress syndrome</span> Human disease

Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). For those who survive, a decreased quality of life is common.

<span class="mw-page-title-main">Pulmonary hypertension</span> Increased blood pressure in lung arteries

Pulmonary hypertension is a condition of increased blood pressure in the arteries of the lungs. Symptoms include shortness of breath, fainting, tiredness, chest pain, swelling of the legs, and a fast heartbeat. The condition may make it difficult to exercise. Onset is typically gradual. According to the definition at the 6th World Symposium of Pulmonary Hypertension in 2018, a patient is deemed to have pulmonary hypertension if the pulmonary mean arterial pressure is greater than 20mmHg at rest, revised down from a purely arbitrary 25mmHg, and pulmonary vascular resistance (PVR) greater than 3 Wood units.

<span class="mw-page-title-main">Cardiogenic shock</span> Medical emergency resulting from inadequate blood flow due to dysfunction of heart ventricles

Cardiogenic shock is a medical emergency resulting from inadequate blood flow to the body's organs due to the dysfunction of the heart. Signs of inadequate blood flow include low urine production, cool arms and legs, and decreased level of consciousness. People may also have a severely low blood pressure and heart rate.

<span class="mw-page-title-main">High-altitude pulmonary edema</span> Human disease

High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). However, cases have also been reported between 1,500–2,500 metres or 4,900–8,200 feet in more vulnerable subjects.

<span class="mw-page-title-main">Hypoxemia</span> Abnormally low level of oxygen in the blood

Hypoxemia is an abnormally low level of oxygen in the blood. More specifically, it is oxygen deficiency in arterial blood. Hypoxemia has many causes, and often causes hypoxia as the blood is not supplying enough oxygen to the tissues of the body.

Cardiac asthma is the medical condition of intermittent wheezing, coughing, and shortness of breath that is associated with underlying congestive heart failure (CHF). Symptoms of cardiac asthma are related to the heart's inability to effectively and efficiently pump blood in a CHF patient. This can lead to accumulation of fluid in and around the lungs, disrupting the lung's ability to oxygenate blood.

<span class="mw-page-title-main">Respiratory disease</span> Disease of the respiratory system

Respiratory diseases, or lung diseases, are pathological conditions affecting the organs and tissues that make gas exchange difficult in air-breathing animals. They include conditions of the respiratory tract including the trachea, bronchi, bronchioles, alveoli, pleurae, pleural cavity, the nerves and muscles of respiration. Respiratory diseases range from mild and self-limiting, such as the common cold, influenza, and pharyngitis to life-threatening diseases such as bacterial pneumonia, pulmonary embolism, tuberculosis, acute asthma, lung cancer, and severe acute respiratory syndromes, such as COVID-19. Respiratory diseases can be classified in many different ways, including by the organ or tissue involved, by the type and pattern of associated signs and symptoms, or by the cause of the disease.

<span class="mw-page-title-main">Alveolar lung disease</span> Medical condition

Alveolar lung diseases, are a group of diseases that mainly affect the alveoli of the lungs.

In medicine, hepatopulmonary syndrome is a syndrome of shortness of breath and hypoxemia caused by vasodilation in the lungs of patients with liver disease. Dyspnea and hypoxemia are worse in the upright position.

Persistent fetal circulation is a condition caused by a failure in the systemic circulation and pulmonary circulation to convert from the antenatal circulation pattern to the "normal" pattern. Infants experience a high mean arterial pulmonary artery pressure and a high afterload at the right ventricle. This means that the heart is working against higher pressures, which makes it more difficult for the heart to pump blood.

Obstructive shock is one of the four types of shock, caused by a physical obstruction in the flow of blood. Obstruction can occur at the level of the great vessels or the heart itself. Causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax. These are all life-threatening. Symptoms may include shortness of breath, weakness, or altered mental status. Low blood pressure and tachycardia are often seen in shock. Other symptoms depend on the underlying cause.

<span class="mw-page-title-main">Transfusion-associated circulatory overload</span> Medical condition

In transfusion medicine, transfusion-associated circulatory overload is a transfusion reaction resulting in signs or symptoms of excess fluid in the circulatory system (hypervolemia) within 12 hours after transfusion. The symptoms of TACO can include shortness of breath (dyspnea), low blood oxygen levels (hypoxemia), leg swelling, high blood pressure (hypertension), and a high heart rate (tachycardia).

<span class="mw-page-title-main">Acute decompensated heart failure</span> Medical condition

Acute decompensated heart failure (ADHF) is a sudden worsening of the signs and symptoms of heart failure, which typically includes difficulty breathing (dyspnea), leg or feet swelling, and fatigue. ADHF is a common and potentially serious cause of acute respiratory distress. The condition is caused by severe congestion of multiple organs by fluid that is inadequately circulated by the failing heart. An attack of decompensation can be caused by underlying medical illness, such as myocardial infarction, an abnormal heart rhythm, infection, or thyroid disease.

Alveolar capillary dysplasia (ACD) is a rare, congenital diffuse lung disease characterized by abnormal blood vessels in the lungs that cause highly elevated pulmonary blood pressure and an inability to effectively oxygenate and remove carbon dioxide from the blood. ACD typically presents in newborn babies within hours of birth as rapid and labored breathing, blue-colored lips or skin, quickly leading to respiratory failure and death. Atypical forms of ACD have been reported with initially milder symptoms and survival of many months before the onset of respiratory failure or lung transplantation.

Swimming induced pulmonary edema (SIPE), also known as immersion pulmonary edema, is a life threatening condition that occurs when fluids from the blood leak abnormally from the small vessels of the lung (pulmonary capillaries) into the airspaces (alveoli).

References

  1. ↑ Dorland's illustrated medical dictionary (32nd ed.). Saunders/Elsevier. 2 May 2011. p. 593. ISBN   978-1-4160-6257-8.
  2. 1 2 3 Assaad S, Kratzert WB, Shelley B, Friedman MB, Perrino A (April 2018). "Assessment of Pulmonary Edema: Principles and Practice" (PDF). Journal of Cardiothoracic and Vascular Anesthesia. 32 (2): 901–914. doi:10.1053/j.jvca.2017.08.028. PMID   29174750.
  3. 1 2 3 4 5 Ware LB, Matthay MA (December 2005). "Clinical practice. Acute pulmonary edema". The New England Journal of Medicine. 353 (26): 2788–2796. doi:10.1056/NEJMcp052699. PMID   16382065.
  4. 1 2 3 Lindow T, Quadrelli S, Ugander M (November 2023). "Noninvasive Imaging Methods for Quantification of Pulmonary Edema and Congestion: A Systematic Review". JACC. Cardiovascular Imaging. 16 (11): 1469–1484. doi: 10.1016/j.jcmg.2023.06.023 . PMID   37632500.
  5. ↑ Guo L, Yang X, Yang B, Tang G, Li C (July 2023). "Prevalence, in-hospital mortality, and factors related to neurogenic pulmonary edema after spontaneous subarachnoid hemorrhage: a systematic review and meta-analysis". Neurosurgical Review. 46 (1): 169. doi:10.1007/s10143-023-02081-6. PMC   10335949 . PMID   37432487.
  6. ↑ Komiya K, Akaba T, Kozaki Y, Kadota JI, Rubin BK (August 2017). "A systematic review of diagnostic methods to differentiate acute lung injury/acute respiratory distress syndrome from cardiogenic pulmonary edema". Critical Care. 21 (1): 228. doi: 10.1186/s13054-017-1809-8 . PMC   6389074 . PMID   28841896.
  7. ↑ Siddiqi TJ, Usman MS, Rashid AM, Javaid SS, Ahmed A, Clark D, et al. (July 2023). "Clinical Outcomes in Hypertensive Emergency: A Systematic Review and Meta-Analysis". Journal of the American Heart Association. 12 (14): e029355. doi:10.1161/JAHA.122.029355. PMC   10382109 . PMID   37421281.
  8. ↑ οἴδημα, οἰδέω . Liddell, Henry George ; Scott, Robert ; A Greek–English Lexicon at the Perseus Project.
  9. ↑ Harper D. "edema". Online Etymology Dictionary .
  10. ↑ Patel MR, Bailey SR, Bonow RO, Chambers CE, Chan PS, Dehmer GJ, et al. (May 2012). "ACCF/SCAI/AATS/AHA/ASE/ASNC/HFSA/HRS/SCCM/SCCT/SCMR/STS 2012 appropriate use criteria for diagnostic catheterization: a report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, Society for Cardiovascular Angiography and Interventions, American Association for Thoracic Surgery, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society of Critical Care Medicine, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance, and Society of Thoracic Surgeons". Journal of the American College of Cardiology. 59 (22): 1995–2027. doi: 10.1016/j.jacc.2012.03.003 . PMID   22578925.
  11. ↑ Rajaram SS, Desai NK, Kalra A, Gajera M, Cavanaugh SK, Brampton W, et al. (February 2013). "Pulmonary artery catheters for adult patients in intensive care". The Cochrane Database of Systematic Reviews. 2013 (2) CD003408: CD003408. doi:10.1002/14651858.CD003408.pub3. PMC   6517063 . PMID   23450539.
  12. 1 2 3 4 5 Vincent J, Moore FA, Bellomo R, Marini JJ, eds. (2024). Textbook of critical care (8th ed.). Amsterdam: Elsevier. ISBN   978-0-323-75929-8.
  13. ↑ What Is Pulmonary Hypertension? From Diseases and Conditions Index (DCI). National Heart, Lung, and Blood Institute. Last updated September 2008. Retrieved on 6 April 2009.
  14. ↑ Adair OV (2001). Cardiology secrets (2nd ed.). Elsevier Health Sciences. Chapter 41, page 210. ISBN   1-56053-420-6.
  15. ↑ Alerhand S, Adrian RJ, Long B, Avila J (August 2022). "Pericardial tamponade: A comprehensive emergency medicine and echocardiography review". The American Journal of Emergency Medicine. 58: 159–174. doi:10.1016/j.ajem.2022.05.001. PMID   35696801. S2CID   248620419.
  16. ↑ MacIver DH, Clark AL (April 2015). "The vital role of the right ventricle in the pathogenesis of acute pulmonary edema". The American Journal of Cardiology. 115 (7): 992–1000. doi:10.1016/j.amjcard.2015.01.026. PMID   25697920.
  17. ↑ Siddiqi TJ, Usman MS, Rashid AM, Javaid SS, Ahmed A, Clark D, et al. (July 2023). "Clinical Outcomes in Hypertensive Emergency: A Systematic Review and Meta-Analysis". Journal of the American Heart Association. 12 (14): e029355. doi:10.1161/JAHA.122.029355. PMC   10382109 . PMID   37421281.
  18. ↑ Siddiqua N, Mathew R, Sahu AK, Jamshed N, Bhaskararayuni J, Aggarwal P, et al. (January 2024). "High-dose versus low-dose intravenous nitroglycerine for sympathetic crashing acute pulmonary edema: a randomised controlled trial". Emergency Medicine Journal. 41 (2): 96–102. doi:10.1136/emermed-2023-213285. PMID   38050078. S2CID   265507643.
  19. ↑ Gandhi SK, Powers JC, Nomeir AM, Fowle K, Kitzman DW, Rankin KM, Little WC (January 2001). "The pathogenesis of acute pulmonary edema associated with hypertension". The New England Journal of Medicine. 344 (1): 17–22. doi: 10.1056/NEJM200101043440103 . PMID   11136955.
  20. ↑ Long B, Koyfman A, Gottlieb M (November 2018). "Management of Heart Failure in the Emergency Department Setting: An Evidence-Based Review of the Literature". The Journal of Emergency Medicine. 55 (5): 635–646. doi:10.1016/j.jemermed.2018.08.002. PMID   30266198. S2CID   52884356.
  21. ↑ Kramer K, Kirkman P, Kitzman D, Little WC (September 2000). "Flash pulmonary edema: association with hypertension and reoccurrence despite coronary revascularization". American Heart Journal. 140 (3): 451–455. doi:10.1067/mhj.2000.108828. PMID   10966547.
  22. ↑ Pickering TG, Herman L, Devereux RB, Sotelo JE, James GD, Sos TA, et al. (September 1988). "Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation". Lancet. 2 (8610): 551–552. doi:10.1016/S0140-6736(88)92668-2. PMID   2900930. S2CID   36141498.
  23. ↑ Hampson NB, Dunford RG (1997). "Pulmonary edema of scuba divers". Undersea & Hyperbaric Medicine. 24 (1): 29–33. PMID   9068153. Archived from the original on 2010-06-17. Retrieved 2008-09-04.{{cite journal}}: CS1 maint: unfit URL (link)
  24. ↑ Cochard G, Arvieux J, Lacour JM, Madouas G, Mongredien H, Arvieux CC (2005). "Pulmonary edema in scuba divers: recurrence and fatal outcome". Undersea & Hyperbaric Medicine. 32 (1): 39–44. PMID   15796313. Archived from the original on September 20, 2008. Retrieved 2008-09-04.{{cite journal}}: CS1 maint: unfit URL (link)
  25. ↑ Kumar M, Thompson PD (May 2019). "A literature review of immersion pulmonary edema". The Physician and Sportsmedicine. 47 (2): 148–151. doi:10.1080/00913847.2018.1546104. PMID   30403902. S2CID   53209012.
  26. ↑ "Transfusion-related acute lung injury (TRALI)". Professional Education. 2016-06-17. Retrieved 2016-12-03.
  27. ↑ Papaioannou V, Terzi I, Dragoumanis C, Pneumatikos I (2009). "Negative-pressure acute tracheobronchial hemorrhage and pulmonary edema". Journal of Anesthesia. 23 (3): 417–420. doi:10.1007/s00540-009-0757-0. PMID   19685125. S2CID   9616605.
  28. ↑ Hines, Roberta L. and Marschall, Katherine. Stoelting's Anesthesia and Co-Existing Disease. 6th edition. 2012. pages 178 and 179.
  29. ↑ "Pulmonary edema". Mayo Clinic . 2018-08-08.
  30. ↑ O'Leary R, McKinlay J (2011). "Neurogenic pulmonary oedema". Continuing Education in Anaesthesia, Critical Care & Pain . 11 (3): 87–92. doi: 10.1093/BJACEACCP/MKR006 . S2CID   18066655.
  31. ↑ "Adverse Reactions". Professional Education. 2016-06-02. Archived from the original on 2016-12-20. Retrieved 2016-12-03.
  32. ↑ Boyle AJ, Mac Sweeney R, McAuley DF (August 2013). "Pharmacological treatments in ARDS; a state-of-the-art update". BMC Medicine. 11: 166. doi: 10.1186/1741-7015-11-166 . PMC   3765621 . PMID   23957905.
  33. ↑ Luks AM (2008). "Do we have a "best practice" for treating high altitude pulmonary edema?". High Altitude Medicine & Biology. 9 (2): 111–114. doi:10.1089/ham.2008.1017. PMID   18578641.
  34. ↑ Bates, M (2007). "High altitude pulmonary edema". Altitude Physiology Expeditions. Retrieved 2008-09-04.
  35. ↑ White J, Gray M, Fisher M (1989). Atrax Robustus IPCS InChem
  36. ↑ Volpicelli G, Elbarbary M, Blaivas M, Lichtenstein DA, Mathis G, Kirkpatrick AW, et al. (April 2012). "International evidence-based recommendations for point-of-care lung ultrasound". Intensive Care Medicine. 38 (4): 577–591. doi: 10.1007/s00134-012-2513-4 . PMID   22392031.
  37. ↑ Light RW, Lee YC (2006-01-01). "PLEURAL EFFUSIONS | Overview". In Laurent GJ, Shapiro SD (eds.). Encyclopedia of Respiratory Medicine. Oxford: Academic Press. pp. 353–358. doi:10.1016/b0-12-370879-6/00299-4. ISBN   978-0-12-370879-3.
  38. ↑ Richalet JP, Gratadour P, Robach P, Pham I, Déchaux M, Joncquiert-Latarjet A, et al. (February 2005). "Sildenafil inhibits altitude-induced hypoxemia and pulmonary hypertension". American Journal of Respiratory and Critical Care Medicine. 171 (3): 275–281. doi:10.1164/rccm.200406-804OC. PMID   15516532.
  39. ↑ Perimenis P (May 2005). "Sildenafil for the treatment of altitude-induced hypoxaemia". Expert Opinion on Pharmacotherapy. 6 (5): 835–837. doi:10.1517/14656566.6.5.835. PMID   15934909. S2CID   24900169.
  40. ↑ Clark, Michael, Kumar, Parveen J. (2009). Kumar and Clark's clinical medicine. St. Louis, Mo: Elsevier Saunders. p. 783. ISBN   978-0-7020-2993-6.
  41. ↑ Fagenholz PJ, Gutman JA, Murray AF, Harris NS (2007). "Treatment of high altitude pulmonary edema at 4240 m in Nepal". High Altitude Medicine & Biology. 8 (2): 139–146. doi:10.1089/ham.2007.3055. PMID   17584008.
  42. ↑ MacIntyre NR (January 2013). "Supporting oxygenation in acute respiratory failure". Respiratory Care. 58 (1): 142–150. doi: 10.4187/respcare.02087 . PMID   23271824.
  43. 1 2 3 4 Cleland JG, Yassin AS, Khadjooi K (February 2010). "Acute heart failure: focusing on acute cardiogenic pulmonary oedema". Clinical Medicine. 10 (1): 59–64. doi:10.7861/clinmedicine.10-1-59. PMC   4954483 . PMID   20408310.
  44. ↑ Berbenetz N, Wang Y, Brown J, Godfrey C, Ahmad M, Vital FM, et al. (April 2019). "Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema". The Cochrane Database of Systematic Reviews. 2019 (4): CD005351. doi:10.1002/14651858.CD005351.pub4. PMC   6449889 . PMID   30950507.
  45. ↑ Zanza C, Saglietti F, Tesauro M, Longhitano Y, Savioli G, Balzanelli MG, et al. (October 2023). "Cardiogenic Pulmonary Edema in Emergency Medicine". Advances in Respiratory Medicine. 91 (5): 445–463. doi: 10.3390/arm91050034 . PMC   10604083 . PMID   37887077.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.