It has a sensitivity of 35% and specificity of 59% (Gibbons RJ  Nitroglycerin: Should We Still Ask? Spontaneous coronary artery dissection remains an unusual cause of acute coronary syndrome. Retrospective study of confirmed MIs:  47% did not present with chest pain, Women and older patients more likely to present without chest pain. A prospective study of 796 ED patients with suspected cardiac chest pain assessed the value of individual historical and examination findings for diagnosing acute myocardial infarction (AMI) and the occurrence of adverse events (death, AMI or urgent revascularization) within 6 months.
A 2-Hour Diagnostic Protocol for Possible Cardiac Chest Pain in the Emergency DepartmentA Randomized Clinical Trial ONLINE FIRST M JAMA Intern Med. Conclusion: Among patients presenting with chest pain to the ED and a history of stress testing within the past 2 years, a normal stress test result was associated with a markedly reduced risk of having a major cardiac endpoint.
Performance of a sensitive troponin assay in the early diagnosis of acute myocardial infarction in the emergency department.Emerg Med Australas. LOW MOLECULAR WEIGHT HEPARINS VERSUS UNFRACTIONATED HEPARIN FOR ACUTE CORONARY SYNDROMES Background This review aimed to identify randomized controlled clinical trials to determine the relative safety and efficacy of subcutaneous low-molecular-weight heparins (LMWH) versus intravenous unfractionated heparin (UFH) for people with acute coronary syndromes (ACS; unstable angina or non-ST segment elevation myocardial infarction). Comment(s) Beta blockade for cocaine induced myocardial infarction has been advocated in some quarters. A majority of those that rule in for MI will have coronary artery blockage (not vasospastic) while a huge majority of those that rule out will have no structural disease. A 9-12 hour observation period with 2 sets negative is probably sufficient if follow-up can be arranged. Can lead to thrombus formation: Although a mural thrombus adheres to the endocardium overlying the infarcted myocardium, superficial portions of it can become detached and produce systemic arterial emboli. After the vascular sheath is removed from the femoral artery, a femoral pseudoaneurysm can form. Picked a group who were admitted, but deemed low risk (<7% by validated risk stratification mechanism), no signs heart failure, hypotension, or arrhythmia. Conclusion:  It might be ok to send home low risk patients after 12 hours, but only if follow up for stress testing or cath can be guaranteed in a timely (24-48 hour) manner. A 2-Hour Diagnostic Protocol for Possible Cardiac Chest Pain in the Emergency DepartmentA Randomized Clinical Trial (JAMA Intern Med.
Deep symmetrical T-wave inversion across the precordial leads may indicate a critical stenosis of the left anterior descending coronary artery (Wellen’s phenomena).
Myocardial infarction (MI) was suspected if the electrocardiogram (ECG) showed ST-segment elevation of 1 mm or more or pathologic Q waves in two or more leads, and these findings were not known to be old. Are serial ECGs useful during the ED evaluation of patients with suspected acute coronary syndromes? Patient Management Recommendations Level A recommendations Do not utilize cardiac serum marker tests to exclude non-AMI acute coronary syndromes (ie, unstable angina).
Relationship of reported sensitivities of various serum markers in relationship to time of symptom onset. CONCLUSIONS: Patients who are symptomatic during acquisition of a normal or nonspecific ECG have rates of adverse cardiovascular events similar to those of patients without symptoms.
Relationship between a Clear-cut Alternative Noncardiac Diagnosis and 30-day Outcome in Emergency Department Patients with Chest Pain Judd E. Objectives: To compare the 30-day event rate in ED chest pain patients whowere diagnosed with a clear-cut alternative noncardiac diagnosiswith the 30-day event rate in the cohort of patients in whoma definitive diagnosis could not be made in the ED.
Conclusions: In the ED chest pain patient, the presence of a clear-cut alternativenoncardiac diagnosis reduces the likelihood of a composite outcomeof death and cardiovascular events within 30 days. It is well known that the main pathogenesis of acute coronary syndromes consists of atherosclerotic plaque disruption and thrombus formation [10]. A unique complication of a right ventricular myocardial infarction is the development of a right-to-left shunt through a patent foramen ovale.  RV infarction causes reduced right ventricular myocardial compliance with increased RV end diastolic and right atrial pressures. The overwhelming symptom of pulmonary edema is difficulty breathing, but may also include coughing up blood (classically seen as pink, frothy sputum), excessive sweating, anxiety, and pale skin. There is no one single test which confirms that breathlessness is caused by pulmonary edema, indeed in many cases the causes of shortness of breath are probably multifactorial. Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. Urgent echocardiography, if available, may strengthen the diagnosis especially in cardiogenic pulmonary edema by demonstrating impaired left ventricular function, high central venous pressures and high pulmonary artery pressures. Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Pulmonary edema is an accumulation of fluid within the parenchyma and air spaces of the lungs. Injury to the lung may also cause pulmonary oedema through injury to the vasculature and parenchyma of the lung. There are also a range of causes of pulmonary edema which are less well characterised and arguably represent specific instances of the broader classifications above. When circulatory causes have led to pulmonary edema, treatment with intravenous nitrates (glyceryl trinitrate), and loop diuretics, such as furosemide or bumetanide, is the mainstay of therapy. High altitude pulmonary edema — (HAPE) is a life threatening form of non cardiogenic pulmonary edema that occurs in otherwise healthy mountaineers at altitudes above 2,500 meters (8,200 feet). Flash pulmonary edema — In medicine, flash pulmonary edema (FPE), is rapid onset pulmonary edema. Ascites is a gastro-enterological term to describe the accumulation of a fluid in the peritoneal cavity which leads to abdominal distension.
Fluid secreted by the liver is exceeded on large scale and the abdominal cavity is distended with such fluid.
In severe or massive ascites patient complains progressive abdominal heaviness, he feels pressure and stiffness of the abdomen, shortness of breath due to pressure on the diaphragm (muscle layer between chest and abdomen. Due to liver cirrhosis, leg swelling and bruising with slight changes in mental behaviour may be noted. Depending on the accumulation of abdominal fluid and its water level, it may be described in three ways. The most common causes is of two types, due to the high Serum Ascites Albumin Gradient (SAAG). The another type is of due to low SAAG, which is extrude type  in which a fluid with high proteins and cellular debris including pus cells, blood, plasma protein, blood cells, white blood cells and platelets may be present, which escapes from vessels and deposited in tissues or tissue surface. Complete Blood Count for basic metabolism, liver enzymes, protein, albumin, cell count,SGOT, SGPT, SAAG etc. Liver – Shrunken with course ecotexture, irregular borders, may appear smaller in size, intrahepatic undilated bilary radicals.
It is only way of prevention in liver is to strictly follow the rules of avoidable and take proper food. Limit on fried foods, oils and its derivatives like ghee, vanaspati ghee- dalda, Milk – as it contains animal fats and is hard to digest, milk derivatives like chass, curd, lassi, paneer, shrikhand, ice creams, deserts, cakes, chocklets, milk cream, etc. Sour and tangy fruits like tomato, kokam, mango, termerind, orange, citrus fruits, etc as it may cause cough and trouble to breathing.
Arogyavardhini Vati – It is used in the treatment of liver diseases, fever, skin diseases, etc.
Gandharvahasthadi Thailam – oil used in the treatment of  bloating, abdominal pain, etc.


Ascites may be cured by Ayurveda without tapping or dialysis, if the treatment is started in early stage. Time duration for getting cure is mostly depends on the strong will power and response of the patient and experience of the practitioner.
If you have few minutes, thank’s for help me and thank’s a lot for all your advise, just hope that one day, I have the chance of meet you in India !!!
PS: By the way we trying all time to give him most of vegetables, fruits and toffu for his food .
Find out what edema really is and how to naturally reduce edema.It is more of a symptom rather than a medical condition.
A loading dose of 0.5 mg per kg may be given by slow intravenous administration (2 to 5 min) for a more rapid onset of action.
Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded.
2 Any type of BBB (right, left, and atypical ? new or old) thought to be obscuring ST-segment analysis in patients with clinical presentation strongly suggestive of AMI.
ST elevation (greater than 0.1 mV, two or more contiguous leads),  time to therapy 12 hours or less, age less than 75 years.
At first sight it would seem to make sense as many of these patients will be hypertensive and suffering the effects of an adrenergic drive.
Although estimates vary based on patient selection, about 10% of mural thrombi result in systemic embolization (2).
Palpation of localized swelling or tenderness in the area, or loss of sensory or motor function, is highly suggestive of hematoma. A pseudoaneurysm is a communication between the femoral artery and the overlying fibromuscular tissue, resulting in a blood-filled cavity.
Derivation of the Four Initial Risk Groups on the Basis of Data Available at the Time of Presentation in the Emergency Department. Ischemia was suspected if the ECG showed ST-segment depression of 1 mm or more or T-wave inversion in two or more leads, and these findings were not known to be old. Level B recommendations Perform repeat ECG or automated serial ECGs during the ED evaluation of patients in whom the initial ECG is nondiagnostic for injury and who have symptoms consistent with ongoing or recurrent ischemia. Exclusion Criteria Contraindications for a glycoprotein inhibitor (bleeding disorder, renal insufficiency, etc).
Clinicians should not rely on the absence of ECG abnormalities during symptoms to help exclude ACS. Data included demographics, medical and cardiac history, laboratory and electrocardiogram results, and whether or not the treating physician ascribed the conditionto a clear-cut alternative noncardiac diagnosis. However,it does not reduce the event rate to an acceptable level toallow ED discharge of these patients. However, no atherosclerotic plaque in the major coronary arteries was detected on coronary angiography.
In patients with an interatrial septal defect, a right-to-left shunt may develop when the right atrial pressure exceeds the left atrial pressure. It is due to either failure of the left ventricle of the heart to adequately remove blood from the pulmonary circulation ("cardiogenic pulmonary edema"), see below, or an injury to the lung parenchyma or vasculature of the lung ("noncardiogenic pulmonary edema"), see below.[2] Whilst the range of causes are manifold the treatment options are limited, and to a large extent, the most effective therapies are used whatever the cause.
In certain circumstances insertion of a Swan-Ganz catheter may be required to aid diagnosis. Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT) are typically requested.
Classically it is cardiogenic (left ventricular) but fluid may also accumulate due to damage to the lung. The cause of pulmonary edema in the presence of a hypertensive crisis is probably due to a combination of increased pressures in the right ventricle and pulmonary circulation and also increased systemic vascular resistance and left ventricle contractility increasing the hydrostatic pressure within the pulmonary capillaries leading to extravasation of fluid and edema.
The patient is given high-flow oxygen, noninvasive ventilation (either continuous positive airway pressure (CPAP) or variable positive airway pressure (VPAP)[12][13]) or mechanical ventilation and positive end-expiratory pressure (PEEP) in very severe cases. The presence of free fluid in the abdominal cavity can only be detected by ultrasound examination. When the abdomen is pressed slightly on one side, it will generate a wave like movement through the fluid which can be noticed on the other side.
It is  transudate type, means, a fluid that passes through a membrane, which filters out of the cells and much proteins yielding watery solution.
Behda, Katuki, Kalmegh, Punarwasu, Guduchi, Kamdudha ras, Praval panchamrut, yashad bhasm, Akik Pishti, Giloy satva, Arjuna, Bhrangaraj, fumaria indica, kasni, vidanga,  milk thistle, goji berry etc. Some studies have reported false-positive elevation of markers for acute myocardial infarction (AMI) in ESRD patients. However, it must be remembered that cocaine affects both alpha and beta receptors and that by giving a beta blocker the effects of alpha blockade on the heart may become unopposed. Indications for surgical intervention include persistent hypotension, decreasing hematocrit despite transfusion, or femoral neuropathy (due to nerve compression). Risk factors included systolic blood pressure below 110 mm Hg, rales heard above the bases bilaterally on physical examination, and known unstable ischemic heart disease, defined as a worsening of previously stable angina, the new onset of postinfarction angina or angina after a coronary-revascularization procedure, or pain that was the same as that associated with a prior myocardial infarction. Patients stratified as moderate risk who also had a high probability of significant coronary artery disease (using the Diamond and Forrester criteria25) were recommended for cardiology consultation. Peaks A, B, and C respectively demonstrate release of myoglobin, troponin, and CK-MB in acute myocardial infarction as defined by WHO diagnostic criteria. The main outcomewas death, acute myocardial infarction (AMI), or revascularizationwithin 30 days, as determined by phone follow-up or medicalrecord review. There was temporary systolic coronary arterial luminal narrowing at the mid-portion of LAD at LAO view.
Such a situation should be suspected in a patient who exhibits significant hypoxemia that is not responsive to the administration of oxygen. Treatment is focused on three aspects, firstly improving respiratory function, secondly, treating the underlying cause, and thirdly avoiding further damage to the lung. The chronic development of pulmonary edema may be associated with symptoms and signs of "fluid overload", this is a non specific term to describe the manifestations of left ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile. B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test. This damage may be direct injury or injury mediated by high pressures within the pulmonary circulation. It may be noticed externally by examining the abdominal structure, visible bulging of the flanks.
Cardiac troponin I (cTnI) has been reported to be specific for cardiac muscle, and is excreted by the kidneys. The sensitivity of the test will be influenced by the amount of METs, the duration of exercise greater than 6?12 min, as well a heart rate at 85% of predicted [1, 2, 3, 4 and 6].
These trials seems to confirm this concern with a decrease in myocardial blood flow and coronary vasoconstriction. Studies suggest that 30 to 60 minutes after baseline may be a reasonable time interval for repeat ECG. Also, it is often considered as a simple variant of the normal anatomy of coronary arteries.
Our patient had a smoking history, and nicotine could have damaged the endothelial structure at the bridged segment.


We have always assumed that when a patient experiences an acute myocardial infraction (AMI), it occurs because of a ruptured plaque followed by coronary thrombosis. Pulmonary edema, especially in the acute setting, can lead to respiratory failure, cardiac arrest due to hypoxia and death.
When directly or indirectly caused by increased left ventricular pressure pulmonary edema may form when mean pulmonary pressure rises from the normal of 15 mmHg[3] to above 25 mmHg.[4] Broadly, the causes of pulmonary oedema can be divided into cardiogenic and non-cardiogenic. In the patient with reclining situation, difference in the percussion note in the flanks which shifts at the time when the patient turns on the other side. Exercise capacity itself shows a linear relation to adverse cardiac outcomes; the greater the METs achieved, the lower the relative risk of events [5]. In a patient with myocardial ischaemia this could result in an even lower coronary blood flow thereby worsening the ischaemia.
Most larger pseudoaneurysms can be treated with ultrasound-guided compression, ultrasound-guided thrombin injection, or surgical repair.
Possible explanation of AMI in our patient could be endothelial injury, severe coronary spasm and finally thrombotic occlusion [11]. Perhaps, the patient can have an AMI due to vasospasm within clean coronaries or coronaries that have minimal stenoses?maybe. METHODS: The authors, from Henry Ford Hospital in Detroit, measured pre- and post- dialysis cTnI in 113 ESRD patients aged 26-92 with no symptoms of acute coronary syndrome who presented for maintenance dialysis.
No evidence was found for difference in occurrence of recurrent angina, or major or minor bleeds. 4 ST depressions greater than or equal to 0.2 mV (2 mm) with upright T-waves in 2 or more contiguous anterior precordial leads (V1 to V4) in patients with clinical presentation suggestive of AMI involving the posterior left ventricular wall. The sensitivity of a standard ETT is thought to be approximately 66%, ranging from 40% to 90%, depending on the severity of disease when compared to the gold standard of coronary angiography, whereas specificity is approximately 84% [6]. However, we must remember that this is a small study in an experimental setting with patients receiving very small amounts of cocaine (much less than the typical recreational user). An emerging alternative therapy is percutaneous polytetrafluoroethylene-covered stent-graft deployment at the site of the pseudoaneurysm.
Stable or unstable angina pectoris, acute myocardial infarction, complete atrioventricular block or sudden death associated with myocardial bridges have been described [8,9]. This is a case of acute myocardial infarction caused by coronary thrombosis in the setting of myocardial bridging.
The common places for edema to occur are feet, ankles and legs.There are cases that edema is caused by a serious medical condition.
Level C recommendations Assess for fibrinolytic therapy in patients with symptoms suggestive of AMI and presenting within 12 hours of symptom onset if ECG reveals: 1 New or presumably new right bundle branch block (RBBB). An arteriovenous (AV) fistula can result from sheath-mediated communication between the femoral artery and femoral vein. A possible association between myocardial bridging and acute myocardial infarction following excess blood donation could not be excluded.
On balance, in light of the feasible pathophysiological argument against the use of beta blockers, and the findings of these limited studies it appears sensible not to advocate the use of beta blockers in acute myocardial pain secondary to cocaine use. An AV fistula may be suggested by the presence of a systolic and diastolic bruit and confirmed by Doppler ultrasonography. This is a report of a case of acute ischemic complication related to myocardial bridging of the LAD, which was resolved by appropriate blood transfusion, and acetylsalicilic acid, beta-blocker, nytroglicerin. So if you the physician are caring for a patient with chest pain that recently had a bnegativeQ catheterization (ie, clean catheterization or a catheterization with insignificant stenoses), then you assume that there is almost no chance that that patient can be having real ACS event.
The blood can be shunted back to your legs, ankles and feet which could cause edema in the lower extremities.Liver Cirrhosis. CLINICAL BOTTOM LINE Beta Blockers should not be used in the treatment of cocaine induced myocardial ischaemia. AV fistulae can be treated with conservative therapy (careful observation) in most patients or with ultrasound-guided compression, surgical repair, or percutaneous implantation of covered stents if necessary. This is a liver disease in which fluid may accumulate in the abdominal cavity and in your lower extremities as a result of alcohol abuse.Kidney disease.
With a diseased kidney, extra sodium and fluid may circulate in your system which could cause swelling of tissues.
CONCLUSIONS: These findings suggest that cardiac troponin I is a reliable marker of myocardial injury in patients with ESRD on chronic dialysis.
Planar Tc99m sestamibi imaging increases the sensitivity to 84%, whereas specificity is 83% [6]. Although this study is not groundbreaking, it does reaffirm what many other studies have indicated: it is very possible, and in fact not infrequent, to have an AMI even in the setting of minimal or no coronary stenosis. Single photon emission computed tomography (SPECT) with Tc99m sestamibi can increase both the sensitivity and specificity to 90% and 93%, respectively [6]. Factors associated with increased risk for stroke include older age, presence of diabetes, saphenous vein graft interventions, and placement of an intra-aortic balloon pump (placed either prophylactically or for intraprocedural complications). The authors analyzed 38,301 patients from a registry (the CRUSADE registry) of patients with non?ST-segment elevation MI who underwent cardiac catheterization to determine the extent of coronary artery disease. The researchers found that 8.6% of these AMI patients had binsignificantQ coronary stenoses (b50% occlusions).
Since there are declining levels of albumin in the blood, fluid will start accumulating.Lymphatic system problems. Since this system helps to clear out fluids that are in excess from the tissues, if this system is damaged, the lymph nodes and lymph vessels that usually drain could possibly have trouble in working correctly.Chronic venous insufficiency. The overall sensitivity of a standard Tc-99 MIBI SPECT is approximately 60?70% in patients with multivessel disease [7 and 9]. These devices can percutaneously place one or more sutures in the femoral artery or deliver a procoagulant, such as collagen or collagen and thrombin, through a sheath to stimulate local hemostasis. Note that these 3 patient factors are the kind of characteristics that are very likely to make us discount the coronary artery disease risk. Additional modalities added to the standard SPECT study, such as echocardiogram or adding pharmacologic agents like dipyridamole, can increase the sensitivity to 82% and 76%, respectively [7 and 9]. Physicians should be aware that hemostasis success rates are less than 100% and that these devices are associated with a risk for vascular complications. These complications include pseudoaneurysm, bleeding and hematoma, infection, arterial stenosis or occlusion, and venous thrombosis. Several reports in the surgical literature suggest that vascular closure devices are associated with a higher incidence of large pseudoaneurysms and pseudoaneurysms not amenable to ultrasound compression therapy, greater loss of blood and need for transfusions, higher incidence of arterial stenosis or occlusion, more extensive surgical repair, and higher incidence of groin infections compared with manual compression. Thus, the possibility of vascular complications should be considered at least as seriously in patients treated with vascular closure devices as in those treated with manual compression.
Avoid foods that contain sodium like processed foods, junk food, olives, soy sauces, pickles, hotdogs, burgers, pizzas and salt as a condiment.
If treatment is done properly, not only will edema be corrected but also the underlying condition if not too severe.There is a list of ways to help treat edema.
Consult with your doctor first about reducing edema before trying out these alternative home remedies to make sure it is safe for you.



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