what is acute cardiopulmonary abnormality?
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It is a general term not specific. It may mean any acute condition related to heart and lungs.\n\nHeart and Lungs are very much inter-related. If any disease affects the heart, the lung is also affected, and vice versa. \n\nThere are certain medical conditions are are Acute and Affect both heart and Lungs e.g. \n->Acute cardiopulmonary Arrest (i.e. sudden stopage of heart and lungs activity like death). \n->Myocardial Infarction with Acute Pulmonary Edema.\n->ARDS (Adult Respiratory Distress Syndrome with Systemic Shock)\n->Pulmonary Embolism with Systemic Shock\n->Pneumothorax with Shock\n->Cardiac Temponade\n(if you want the detail of above medical condition you can visit:\nhttp://www.nlm.nih.gov/medlineplus/encyclopedia.html\nThere are also many other Acute Medical Emergencies those involve the cardiopulmonary abnormalities. \n\nIf you are not a medical person and to answer briefly, i would like to say that it is any sudden abnormality realted to heart and lungs.
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It means behind the heart.  Usually referred to something seen on a chest xray, often a pneumonia or other lung infiltrate that is behind the heart.
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heart attack during sleep\nsupposedly
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air is moved into the lungs
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The American College of Chest Physicians (ACCP) is a medical specialty society of physicians, surgeons, allied health professionals, and individuals with PhD degrees who specialize in diseases of the chest: pulmonology, cardiology, cardiovascular and cardiothoracic surgery, hypertension, critical care medicine, and related disciplines.\n\nThe ACCP creates a unique multidisciplinary approach to cardiopulmonary medicine where pulmonologists, cardiologists, thoracic surgeons, and others can come together at College events for an experience not available from other sources—examination of a topic from a perspective that encompasses all of the major specialties involved.
287073
acute lead poisoning?
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It means that there is a trivial amount of backflow of blood thru both of these valves. The abnormal flow of blood is backwards from the ventricles back to the atria, I use the pleural because it involves 2 valves. Only you know if this medical information will keep you off the force, and since it is so small, it may not even show up as a heart murmur. To put your mind at ease you would want to talk to a doctor, but it does not sound like it is a problem currently. Check back when you get older as heart valves tend to get stiffer, and calcify with age and this may become a larger leak as you age.
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A lung disease caused by extremely small particles of Volcanic ash and dust..\n\nI din't have to google it, i knew it ;).. i read it in a book long time ago. I even have the book now, so i gave you the exact defination from the book :)
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Increased Bronchovascular Markings\n\nThis always means either infection in respiratory passages or fluid overload. Infection may be acute or chronic. If radiologist reports increased bronchovascular markings but clinical situation is not supporting any thing it can be ignored and film should be taken as normal.\n\nIn cardiac failure cases so called reversal of pattern of markings occur. There is increase in markings in midzones due to fluid overload. Actually this is not reversal. This is only increase in midzones.\n\nIn chronic bronchitis, markings are increased. In emphysema, these are decreased in hyperinflated areas. In collapse of the lungs beyond the line-demarcating lung, these must be absent.
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Background: Ch'in and Tang first described cystic adenomatoid malformation (CAM) as a distinct entity in 1949. CAM is a developmental hamartomatous abnormality of the lung with adenomatoid proliferation of cysts resembling bronchioles. CAM represents approximately 25% of all congenital lung lesions.\n\n\nPathophysiology: \n\n\nPathogenesis and pathophysiologic features \n\nCAM is believed to result from focal arrest in fetal lung development before the seventh week of gestation secondary to a variety of pulmonary insults. Depending on the time and type of insult, 4-26% of cases can be associated with other congenital abnormalities. However, arrest of pulmonary development with distortion of architectural differentiation may take place at any stage of embryonic development. \n\nCAM differs from normal lung tissue because of a combination of increased cell proliferation and decreased apoptosis. A well-defined intrapulmonary bronchial system is lacking, and normally formed bronchi supplying the mass are absent. \n\nTypes of CAM \n\nCAM is subdivided into 3 major types. \n\nType I lesions, the most common, are composed of 1 or more cysts measuring 2-10 cm in diameter. Larger cysts are often accompanied by smaller cysts, and their walls contain muscle, elastic, or fibrous tissue. Cysts are frequently lined by pseudostratified columnar epithelial cells, which occasionally produce mucin. Mucinogenic differentiation is unique to this subtype of CAM. \n\nType II lesions are characterized by small relatively uniform cysts resembling bronchioles. These cysts are lined by cuboid-to-columnar epithelium and have a thin fibromuscular wall. The cysts generally measure 0.5-2 cm in diameter. \n\nType III lesions consist of microscopic, adenomatoid cysts, and are grossly a solid mass without obvious cyst formation. Microscopic adenomatoid cysts are present. \n\nCAM receives its blood supply from the pulmonary circulation and is not sequestered from the tracheobronchial tree. However, type II and III lesions can occasionally coexist with extralobar sequestration, and in such cases, they may receive systemic arterial supply. CAM may also occur in combination with a polyalveolar lobe. A polyalveolar lobe is a form of congenital emphysema with increased number of alveoli with normal bronchi and pulmonary vasculature. CAM usually occurs early in fetal life, whereas polyalveolar lobe occurs late. \n\nDifferential diagnosis \n\nCAM is differentiated from other congenital cystic disease by 5 characteristics including the following: (1) absence of bronchial cartilage (unless it is trapped within the lesion); (2) absence of bronchial tubular glands; (3) presence of tall columnar mucinous epithelium; (4) overproduction of terminal bronchiolar structures without alveolar differentiation, except in the subpleural areas; and (5) massive enlargement of the affected lobe that displaces other thoracic structures.\n\n\nFrequency: \n\n\nInternationally: In Canada, the estimated incidence of CAM is 1 case per 25,000-35,000 pregnancies. \nMortality/Morbidity: The prognosis primarily depends on the size of the lesion. In a Canadian series of 48 patients, the incidence of postnatal demise was 10% (10 of 40 patients) with 8 spontaneous and voluntary abortions. Larger lesions have a higher incidence of mediastinal shift, vascular compromise, polyhydramnios, pulmonary hypoplasia, and hydrops, which may lead to intrauterine fetal demise or neonatal death. \n\nType III CAM tends to be extensive and therefore tends to have a poor prognosis. The prognosis is also poor with bilateral lung involvement, prematurity, and severe associated malformations. The most commonly associated anomalies occur in the type II form. The anomalies affect the renal (cystic disease, agenesis, dysgenesis), intestinal (atresias), cardiac, and osseous systems. \n\nWhen CAM is identified in utero, as many as 56% of the lesions detected can regress spontaneously, although initially, they may progr
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By what information you have given me my 1st guess would be cardiogenic shock. But you don't say why the thoracotomy was preformed. Was it for heart, heart valves, lung, thorasic aorta, esphageal or spine surgery. You also don't say wether this patient had a cardiac or pulmonary arrest or if both which occured 1st. I chose cardiogenic shock 1st due to all the already existing cardiac issues and additional symptoms. Was the CHF ( which  pulmonary edema is a symptom) caused by the cardiomegaly , the A-fib, the MV prosthesis or a combination of some or all. You also mentioned a previous CABG, but you didn't mention any myocardial injury occuring. This pt. not only had mechanical issues but also had electrical problems as demonstrated by the A-fib and the RBBB. The pulmonary involvement sounds more like it's due to all the cardiac problems. You mentioned hypotention but not whether it was due to medication or if it was a symptom of the cardiomegaly. You mentioned oliguria but nothing of CRF or even ARF post surgery. So was this a new onset? You give no lab values that could indicate organ functions. Sooooooooo. I still stand with cardiogenic shock as my 1st choice (chosen from all the cardiac envolvement and the possibility that he could have thrown a clot [a-fib, PMV and had to be taken off thinners for the surgery] and had an MI. The symptoms of hypotention & oliguria occur in cardiogenic shock). My 2nd choice would be a CVA ( due to the A-fib the PMV and the fact he had to be off anticoagulants for the thoracotomy. 3rd and lastly alcohol withdrawal (just kidding! Really I was just kidding!)
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Hi, catherine - It sounds like your question basically boils down to semantics.  When someone is in congestive heart failure, their level of activity is limited by shortness of breath or fatigue.  Usually this is a result of abnormal heart function (a 'cardiomyopathy'), but once they are adequately treated and feel back to normal again, they are technically no longer IN congestive heart failure.  But they still have a cardiomyopathy because the underlying problem has not changed.  So you COULD say that congestive heart failure is a clinical condition, but the cardiomyopathy is the underlying disease.  You could argue that either way, though...
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Rheumatic fever (RF) is an illness characterized by the presence of one or more of the following findings: arthritis, carditis (cardiac inflammation), rash, chorea (abnormal movements), and subcutaneous nodules. The clinical manifestations are a direct consequence of a throat infection caused by the group A beta-hemolytic Streptococcus bacteria, which causes Strep throat.\nSubcutaneous nodules are small (less than 1 cm) bumps, found mostly over bony areas, usually seen in recurrent attacks, and have an incidence of about 3-10%. Patients who have nodules usually also have severe heart disease. Nodules usually disappear in 1-2 weeks.
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hahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahaahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahaahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahaahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahahaahahahahahaha. Call an ambulance hahahahah i'm having a heart attack
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The heart beats in an irregular beating pattern...From the lungs to causing you to release air in a odd pattern sending of noises...
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Pathophysiology: As a group, regardless of etiology, a common pathophysiology exists that begins with acute injury to the pulmonary parenchyma, leading to chronic interstitial inflammation, and ultimately progressing to the common end point of pulmonary fibrosis and tissue destruction. \n\nThe DPLDs typically manifest with the insidious onset of respiratory symptomatology, although onset can be acute and rapidly progressive, as in bronchiolitis obliterans-organizing pneumonia (BOOP) or acute interstitial pneumonitis. \n\nPathologically, all manifest histologically with disease in the interstitial compartment of the lung. The histologic patterns of usual interstitial pneumonitis (UIP), desquamative interstitial pneumonitis (DIP), nonspecific interstitial pneumonitis, hypersensitivity pneumonitis (HSP), lymphocytic interstitial pneumonitis, BOOP, giant cell pneumonitis, and granulomatous pneumonitis are most common and are centered in the alveolar, lobular, and lobar septa, impacting alveoli, small airways, and pulmonary vasculature.
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lack of oxygen and poor circulation