Pulmonary edema | |
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Other names | Pulmonary oedema |
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 |
Causes | Cardiogenic, Noncardiogenic (pneumonia, inhalation injury, sepsis, airway obstruction, high altitude) |
Diagnostic method | Medical imaging, lab tests, ECG, echocardiography |
Treatment | Supplemental 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 shortness of breath (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]
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:
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]
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 physicians to classify and subsequently treat the underlying cause of pulmonary edema.
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]
The term pulmonary edema literally means wet lungs. This term actually refers to a pathological condition of the lungs, frequently demonstrated by chest X-ray. Edema of the lungs should be thought of as the result of a disease such as congestive heart failure and not a disease in and of itself. In this case it would be a cardiac disease and not a pulmonary disease.
Cardiogenic pulmonary edema is typically caused by either volume overload or impaired left ventricular function. As a result, pulmonary venous pressures rises from the normal average of 15 mmHg. [13] As the pulmonary venous pressure rises, these pressures overwhelm the barriers and fluid enters the alveoli when the pressure is above 25 mmHg. [14] Depending on 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 is a clinical syndrome that begins suddenly and accelerates rapidly. Essentially all patients will present to the emergency department by ambulance.
The initiating acute event often a vascular event such as intense vasoconstriction and not a cardiac event such as myocardial infarction. 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 are often not recognized as having a cardiovascular disease. Treatment of FPE should include reducing systemic vascular resistance with nitroglycerin, providing supplemental oxygenation, and decreasing left ventricular filling pressure. Effective treatment is evident by a decrease in dyspnea and normalization of vital signs. Important targets of therapy such as reduced systemic vascular resistance and reduced left atrial pressure are difficult if not impossible to monitor. [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 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.
Acute lung injury may cause pulmonary edema directly through injury to the vasculature and parenchyma of the lung, causes include:
Some causes of pulmonary edema are less well characterized and arguably represent specific instances of the broader classifications above.
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) 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.
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.
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]
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.
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]
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 is the result of cardiovascular insufficiency. Treatment is directed at improving cardiovascular function and providing supportive care. [43] [44] Positioning upright may relieve symptoms. A loop diuretic such as furosemide is administered, often together with morphine to reduce respiratory distress. [44] 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. [44]
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. [45]
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. [44]
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. [46]
Cardiology is the study of the heart. Cardiology is a branch of medicine that deals with disorders of the heart and the cardiovascular system. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease, and electrophysiology. Physicians who specialize in this field of medicine are called cardiologists, a sub-specialty of internal medicine. Pediatric cardiologists are pediatricians who specialize in cardiology. Physicians who specialize in cardiac surgery are called cardiothoracic surgeons or cardiac surgeons, a specialty of general surgery.
Edema, also spelled oedema, and also known as fluid retention, dropsy and hydropsy, is the build-up of fluid in the body's tissue, a type of swelling. Most commonly, the legs or arms are affected. Symptoms may include skin that feels tight, the area feeling heavy, and joint stiffness. Other symptoms depend on the underlying cause.
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 state of consciousness due to ischemia in the brain.
Shortness of breath (SOB), known as dyspnea or dyspnoea, is an uncomfortable feeling of not being able to breathe well enough. The American Thoracic Society defines it as "a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity", and recommends evaluating dyspnea by assessing the intensity of its distinct sensations, the degree of distress and discomfort involved, and its burden or impact on the patient's activities of daily living. Distinct sensations include effort/work to breathe, chest tightness or pain, and "air hunger". The tripod position is often assumed to be a sign.
Heart failure (HF), also known as congestive heart failure (CHF), is a syndrome caused by an impairment in the heart's ability to fill with and pump blood.
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.
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.
Orthopnea or orthopnoea is shortness of breath (dyspnea) that occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair. It is commonly seen as a late manifestation of heart failure, resulting from fluid redistribution into the central circulation, causing an increase in pulmonary capillary pressure and causing difficulty in breathing. It is also seen in cases of abdominal obesity or pulmonary disease. Orthopnea is the opposite of platypnea, shortness of breath that worsens when sitting or standing upright.
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.
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). HAPE is a severe presentation of altitude sickness. Cases have also been reported between 1,500–2,500 metres or 4,900–8,200 feet in people who are at a higher risk or are more vulnerable to the effects of high altitude.
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.
Alveolar lung diseases, are a group of diseases that mainly affect the alveoli of the lungs.
The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.
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.
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).
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).
Pulmonary artery agenesis refers to a rare congenital absence of pulmonary artery due to a malformation in the sixth aortic arch. It can occur bilaterally, with both left and right pulmonary arteries being absent, or unilaterally, the absence of either left or right pulmonary artery (UAPA). About 67% of UAPA occurs isolated in the right lung. The absence of pulmonary artery can be an isolated disorder, or accompanied by other related lesions, most commonly Tetralogy of Fallot.