Sodium heparin is reserved for cases in which the patient is stable.

The patient presented pulmonary thromboembolism which, in addition to being bilateral, produced severe hemodynamic involvement, shock and required mechanical ventilation. We are not told that he has any contraindication to fibrinolysis, so this would be the most appropriate option due to its rapid administration and action. Sodium heparin is reserved for cases in which the patient is stable. Thromboendarterectomy could be performed urgently in selected centers (not available in all) in patients in whom systemic fibrinolysis is contraindicated, or in centers where the experience with this technique is proven and it can be performed quickly. The inferior vena cava filter is a treatment indicated in the acute phase in stable patients, when anticoagulation is contraindicated; or a posteriori, as prophylaxis, in this group of patients. The indications for fibrinolysis in the last SEPAR consensus document included patients at intermediate risk (they could benefit from it) and high risk. They classify intermediate risk as PESIs ≥ 1 or PESI III-IV. In this subgroup, patients with right ventricular dysfunction, troponin or BNP above the cutoff and deep vein thrombosis appear to benefit most from fibrinolysis. In the subgroup of high-risk patients (defined by hypotension or cardiogenic shock criteria), the use of systemic fibrinolysis is much clearer, as in the case presented in the question.

The patient presented pulmonary thromboembolism which, in addition to being bilateral, produced severe hemodynamic involvement, shock and required mechanical ventilation. We are not told that he has any contraindication to fibrinolysis, so [HIDDEN] due to its rapid administration and action. Sodium heparin is reserved for cases in which the patient is stable. Thromboendarterectomy could be performed urgently in selected centers (not available in all) in patients in whom systemic fibrinolysis is contraindicated, or in centers where the experience with this technique is proven and it can be performed quickly. The inferior vena cava filter is a treatment indicated in the acute phase in stable patients, when anticoagulation is contraindicated; or a posteriori, as prophylaxis, in this group of patients. The indications for fibrinolysis in the last SEPAR consensus document included patients at intermediate risk (they could benefit from it) and high risk. They classify intermediate risk as PESIs ≥ 1 or PESI III-IV. In this subgroup, patients with right ventricular dysfunction, troponin or BNP above the cutoff and deep vein thrombosis appear to benefit most from fibrinolysis. In the subgroup of high-risk patients (defined by hypotension or cardiogenic shock criteria), the use of systemic fibrinolysis is much clearer, [HIDDEN].

A 58-year-old man, three weeks after a severe ankle sprain presents, rapidly progressive, with dyspnea at rest, dizziness and syncope. On arrival at the hospital he has hypotension (systolic BP 80 mmHg, diastolic 40 mmHg) and poor perfusion. He is intubated and connected to mechanical ventilation and noradrenaline is started. Echocardiogram shows signs of pulmonary hypertension. Angio-CT shows multiple repletion defects occupying both main pulmonary arteries. Which of the following treatments would be associated with the most rapid hemodynamic improvement in this case?

Systemic fibrinolysis with rt-PA (alteplase) 100 mg intravenous.

Mechanical and enzymatic thrombolysis for massive pulmonary embolism.

To assess the efficacy and safety of mechanical fragmentation combined with intrapulmonary thrombolysis in massive pulmonary thromboembolism (PTE) with hemodynamic impairment. Fifty-nine patients diagnosed with massive PTE with hemodynamic impact were treated. The initial clinical symptoms were shock in 23 patients (38.9%), syncope in eight (13.5%), and dyspnea at rest in 28 (47.4%). Mean O2 saturation was 67.8%. Mean pulmonary artery pressure (PAP) was 42.1 mm Hg. During fragmentation, thrombolysis was administered in the form of a urokinase bolus of 200,000-500,000 U in 57 patients and 20 mg of recombinant tissue plasminogen activator (rt-PA) in two patients. The mean urokinase dose used was 2,500,000 IU, whereas the total dose of rt-PA was 100 mg. Heparin sodium infusion was performed to reach activated partial thromboplastin time ratios of 2. The follow-up consisted of clinical assessment, pulmonary scintigraphy, and echocardiography. The patients received treatment with dicoumarin for 6 months after the procedure. Clinical improvement was seen in 56 patients (94%). Three patients died. The mean PAP after the treatment was 21.8 mm Hg. The mean posttreatment Miller index was 0.35. Technical success was achieved in all cases and clinical symptoms improved in all cases except those in which the patients died. Pulmonary scintigraphy showed improved perfusion in all cases. Echocardiography was performed after 3-6 months, showing a mean pressure of 22.8 mm Hg (corrected values). There were no signs of recurrent PTE or arterial hypertension in the follow-up. The data provided confirm the efficacy and safety of mechanical fragmentation and pharmacologic thrombolysis in the treatment of massive PTE with hemodynamic impairment, showing improvement of symptoms and a decrease in PAP.

[Acute pulmonary thromboembolism with severe hemodynamic compromise. The efficacy of systemic thrombolytic treatment in the coronary unit].

A 79[correction of seventy]-year-old patient, who has been in bed a long time, suffered an episode of sudden dyspnea, tachycardia and tachypnea. An electrocardiogram registered at her admission in the coronary care unit showed a normal rhythm with right axis deviation and S1Q3T3 pattern and ST segment alterations. A ventilation-perfusion lung scanning demonstrated segmental perfusion defects with high probability of pulmonary embolism. She developed a low cardiac output syndrome, which neither responded to the volume expansion nor to the inotropic drugs. The bed-side hemodynamic measurements were a systolic pulmonary pressure of 60 mmHg, with a diastolic pressure of 18 mmHg and capillary wedge pressure of 13 mmHg with high pulmonary resistance. With this evidences, the diagnoses of massive pulmonary embolism was done, thrombolytic treatment was decided on. Two hundred and fifty thousands international units of streptokinase was administered, and then 100.000 UI/hour in 24 hours; after that with intravenous heparin. The low cardiac output syndrome disappeared. The patients recovered her systemic arterial pressure and her diuresis. The electrocardiographic signs vanished and both the pulmonary pressure and resistance decreased. We discussed the importance of intravenous thrombolytic treatment in massive pulmonary embolism. We concluded than this treatment is an useful strategy that not always needs a pulmonary arteriography, and could be used in low complexity centres, successfully in the massive pulmonary thromboembolism with severe hemodynamic damage.

[High doses and the rapid infusion of streptokinase for the treatment of massive pulmonary thromboembolism].

We report the case of a 65 year old woman with no prior cardiac or pulmonary disease, who suffered pulmonary embolism (PE); diagnosis was made on the basis of the existence of risk factors, clinical, radiographic and electrocardiographic features, and a lung scan with perfusion defects and normal ventilation. PE was considered massive because the patient developed acute respiratory failure that required tracheal intubation and mechanical ventilation as well as obstructive shock, electrocardiographic and echocardiographic data of right ventricle overload, and pulmonary hypertension, with pulmonary artery pressure of 38 mmHg. She received an initial treatment with high doses (1,500,000 UI) and rapid infusion (1 hr) of intravenous streptokinase (SK) followed by heparin anticoagulation. Thereafter the hemodynamic disturbances improved and pulmonary artery pressure post-thrombolysis was 23 mmHg. In this report SK at high doses and rapid infusion showed effectiveness and security. We emphasize the usefulness of echocardiography as a diagnostic aid in patients with a previously healthy cardiopulmonary system, as well as the possible role of electrocardiogram as an early indicator of pulmonary reperfusion. This could be the first report of successful thrombolysis with high doses and rapid infusion of SK in massive PE.

Rapid dynamic bedside assessment of pulmonary perfusion defect by electrical impedance tomography in a patient with acute massive pulmonary embolism.

Several animal studies have shown that regional lung perfusion could be effectively estimated by the hypertonic saline contrast electrical impedance tomography method. Here, we reported an application of this method to dynamically assess regional pulmonary perfusion defect in a patient with acute massive pulmonary embolism. A 68-year-old man experienced sudden dyspnea and cardiac arrest during out-of-bed physical activity on the first day after partial mediastinal tumor resection. Acute pulmonary embolism was suspected due to acute enlargement of right heart and fixed inferior venous cava measured with bedside ultrasound. The computed tomography pulmonary angiography further confirmed large embolism in both left and right main pulmonary arteries and branches. The regional time impedance curves, which were obtained by a bolus of 10 ml 10% NaCl through the central venous catheter, were then analyzed to quantitatively assess regional perfusion. Normal ventilation distribution with massive defects in regional perfusion in both lungs was observed, leading to a ventilation-perfusion mismatch and low oxygenation index (PaO<sub2</sub/FiO2 = 86 mmHg) at the first day of pulmonary embolism. The anticoagulation was performed with heparin, and the patient's condition (such as shock, dyspnea, hypoxemia, etc.), regional lung perfusion defect, and ventilation-perfusion mismatch continuously improved in the following days. In conclusion, this case implies that electrical impedance tomography might have the potential to assess and monitor regional perfusion for rapid diagnosis of fatal pulmonary embolism in clinical practice.

High-risk pulmonary embolism assessed by transthoracic echocardiography: A case report.

Acute pulmonary embolism (APE) as a life-threatening illness may present with a wide range of manifestations. APE was diagnosed using computed tomographic pulmonary angiography (CTPA); however, transthoracic echocardiography (TTE) can reveal hemodynamic status. Early thrombolysis is the most effective therapy for the treatment of massive pulmonary embolism. Herein, we report a case of high-risk APE with a wide range of manifestations, including chest pain, dyspnea, low-blood pressure, and syncope. A 55-year-old, previously healthy woman, complained of dyspnea and pleuritic chest pain for 40 days, along with transitory (10 minutes) episodes of syncope that had occurred 2 days previously. Because of the high-risk APE, the patient received intravenous thrombolytic therapy with low-dose recombinant tissue plasminogen activator (rt-PA, 50 mg over 30 minutes) and an anticoagulant (subcutaneous low-molecular-weight heparin, once every 12 hours for 5 days). Five days after thrombolysis, bedside TTE revealed RV diastolic dimension decreased to 22 mm. Color ultrasonography revealed a significant decrease in systolic and mean pulmonary artery pressure. TTE may provide initial suspicion of APE and may help identify patients with unstable hemodynamic status before the onset of shock. Moreover, concomitant TTE signs of decreased RV load may predict better prognosis for high-risk APE patients.

[Pulmonary thromboembolism. A clinical case with unusual presentation].

The authors describe a rare case of pulmonary thromboembolism with unusual clinical findings and emphasized the large difficulty encountered in formuling a correct diagnosis in a reasonable time. A man, 60 years old, was admitted to a Medical Division of our hospital for the appearance of chest pain and epigastric pain during effort in the last year. He smoked 20 cigarettes a day and drank wine (1 or 2 litres a day). He was affected by hypercholesterolemia and in the past reported relapsed thrombophlebitis in the left leg. Four years before admission to our hospital he underwent large and small left saphenectomy. He had no cardiac events in the past. After a non significant exercise stress test the patient was treated with nitrates and asa and was discharged from the hospital. At home the symptoms increased and after 8 months the patient was admitted again to the Cardiologic Division of the hospital. At admission he reported dyspnea and chest pain at rest, not only during effort and the ECG showed negative T waves in anterior and inferior leads. Intravenous heparine, nitrates and calcium antagonists stabilized the clinical picture. The following examinations revealed: reduction of the T wave negativity at the ECG registered during chest pain; mild enlargement of the heart at the chest roentgenogram; normal value of the left ventricle and apical and midseptal by ipokinesia at the transthoracic echocardiogram; normal coronary artery at the coronary arteriography. "Vasospastic angina" was diagnosed and the patient was discharged after 20 days, asymptomatic. After 15 days he returned to the hospital again for chest pain, dyspnea, hypotension and syncope despite therapy. At physical examination he showed a painful left tibio-tarsal tumefaction, an increased and splitting second heart sound in the pulmonary area and a systolic murmur in the third and fourth left interspace. The ECG showed a severe anterior ischemia, while a new transthoracic echocardiogram revealed a considerable dilatation of the right atrium, right ventricle and the main pulmonary artery with severe tricuspid regurgitation and pulmonary hypertension (mean PAP about 50 mmHg). The following pulmonary perfusion scintigraphy confirmed the diagnosis of pulmonary embolism and the selective right and left pulmonary arteriography exhibited multiple thrombi and large intravascular filling defects. The right heart catheterization confirmed a chronic precapillary pulmonary hypertension (mean PAP = 55 mmHg). About 24 hours after these examinations the patient died because of a cardiac arrest with electromechanical dissociation. Pulmonary thromboembolism is a potentially fatal disease characterized by a largely variable clinical presentation. Frequently pulmonary embolism diagnosis is difficult especially when clinical findings are unusual. In the case observed the "typical" chest and epigastric pains associated with the electrocardiographic findings directed diagnosis towards myocardial ischemia. Also after the coronary arteriography that showed normal coronary artery, the erroneous diagnosis persisted. Pulmonary embolism was correctly diagnosed too late to begin an effective therapy. These unusual clinical findings and diagnostic mistakes are stressed and critically reviewed in the article.

[A case of large pulmonary embolism in trunk and branches with main manifestation of syncope, vomiting and shock].

Pulmonary embolism (PE) refers to the endogenous or exogenous emboli blocking pulmonary trunk or branches, causing clinical and pathophysiological syndrome of pulmonary circulation disorder, the incidence rate is high. Sometimes PE patients were lack of specific symptoms and signs, or without any symptoms, which often result in misdiagnosis, un-timely diagnosis, and the delay of treatment. A PE case with syncope, vomiting and shock, which was proved to be pulmonary artery trunk and branch wide embolism later, was presented so as to improve the understanding of the disease.

Anterior cerebral artery syndrome

Management Pulse oximetry can guide the use of supplemental oxygen to maintain oxygen saturation greater than 94%. Hyperoxia should be avoided as may be detrimental in stroke. Hypertension is common in an acute ischemic stroke. A low BP is uncommon and may indicate symptoms exacerbation of a previous stroke due to poor perfusion. Blood pressure of 220/120 mmHg should receive treatment. There is a consensus approach of allowing permissive hypertension up to 220/120 mmHg for patients that are not candidates for thrombolysis.[21] However, for a patient that is a potential candidate for alteplase, attempt to control BP should be made immediately as goal BP for initiation of IV alteplase is 185/110 mmHg. Usually, titratable short-acting intravenous hypotensive agents are recommended to avoid dropping the BP too much once the patient is at goal. Hypotensive agents that can be options include labetalol, nicardipine, clevidipine, hydralazine, enalaprilat.[21]

[Massive pulmonary thromboembolism treated successfully with streptokinase. Report of one case].

Massive pulmonary thromboembolism has a high mortality. Early thrombolysis is the treatment of choice. We report a 79-year-old man admitted in shock. A chest angio-CAT scan showed a massive pulmonary thromboembolism. A transthoracic echocardiography showed a right cardiac dysfunction. Although the patient was in hemodynamic instability, he was subjected to thrombolysis with streptokinase, assisted with noradrenaline support and invasive mechanical ventilation. Parenteral anticoagulation was started thereafter. A second echocardiography, performed 72 hours later showed an improvement in right ventricular function. The patient had a nosocomial pneumonia that was treated. Noradrenalin and mechanical ventilation were discontinued nine and 15 days after thrombolysis. A new angio-CAT scan, 23 days after the procedure, was normal. The patient was discharged in good conditions 27 days after admission.

[A case of primary pulmonary artery myxosarcoma associated with severe pulmonary hypertension].

A 50-year-old man presented with progressive dyspnea on exertion, but with no history of chest pain or syncope. Chronic pulmonary thromboembolism was suspected and he was referred to our hospital. On ausculation, a grade 3 systolic murmur was heard, that was loudest in the fifth intercostal space lateral to the right sternal border. Chest radiography showed mild cardiomegaly and ventilation-perfusion scan revealed absence of perfusion in the left lung and the upper field of the right lung. Contrast-enhanced helical CT showed large mural defects in both main pulmonary arteries, clearly delineated by contrast medium. The left pulmonary artery was nearly completely occluded, and eccentric defects were observed projecting into the lumen of the pulmonary trunk. A tumor originating in the pulmonary artery was suspected, but a definitive diagnosis of the mass could not be made with pulmonary angiography and magnetic resonance imaging. The mean pulmonary arterial pressure was 50 mmHg. Further radiologic examinations failed to reveal the source of the embolus or tumor. It was decided to attempt surgical excision under total cardiopulmonary bypass. At operation, a gelatinous, lustrous, yellowish mass was found partially occluding the right main pulmonary artery and completely occluding the left. The tumor adhered tightly to the intima of the vessel and was inoperable. The patient could not be weaned from percutaneous cardiopulmonary support and died 3 days after surgery. Histologic examination of the excised specimen revealed myxosarcoma.

[A case of successful pulmonary embolectomy for massive acute pulmonary thromboembolism].

A 54-year-old man was admitted to our hospital complaining of sudden-onset dyspnea in shock. Chest computed tomography(CT) showed thrombi in the right main and left intermediate pulmonary arteries. The case was diagnosed as a massive acute pulmonary thromboembolism. Although his hemodynamic status was stable after catecholamine infusion, his dyspnea was still in progress. Emergency pulmonary embolectomy was performed and the life of patient was saved. It is thought that progressive dyspnea is an important sign of a deteriorating hemodynamic status and the predictive symptom indicating a surgical procedure in patients with massive acute pulmonary thromboembolism.

[A case of pulmonary thromboembolism due to idiopathic thrombosis of inferior vena cava, which was initially misdiagnosed as pneumonia].

We report a case of a 73-year-old man with pulmonary embolism due to idiopathic thrombosis of the inferior vena cava. He was referred to our hospital because of a fever and cough of 2 weeks' duration despite treatment with an oral antibiotic. Chest radiography on the first visit showed an infiltrate in the right middle lung field. He was diagnosed as having pneumonia and admitted to our hospital for treatment. Following administration of intravenous antibiotics, his symptoms disappeared and the chest radiography findings improved. The abdominal CT obtained in an attempt to visualize the cause of liver dysfunction serendipitously revealed thrombosis of the inferior vena cava, which was suspected to have caused the pulmonary embolism. A subsequent lung perfusion scan revealed marked perfusion defects in the right middle and lower lobes. Chest CT revealed an embolus located in the right pulmonary artery. Since thrombolytic therapy was not effective, the placement of a filter in the inferior vena cava was performed to prevent the recurrence of pulmonary embolism. The patient has been asymptomatic without recurrence of the disease since the filter insertion.

[Differences in patients with chronic pulmonary embolism and primary pulmonary hypertension].

Chronic pulmonary embolism is a rare disease which can occur at first with pulmonary hypertension. In these cases it may be difficult to distinguish between primary pulmonary hypertension. We examined nine patients with Chronic Pulmonary Embolism (CPE) (three females and six males, mean age 45 +/- 13 years, range 21-67 years) and ten patients with Primary Pulmonary Hypertension (PPH) (seven females and three males, mean age 35 +/- 13 years, range 10-56 years) who came to our attention during the years 1973-1986 (mean follow up 3 years). All patients had an electrocardiogram, chest x-ray, echocardiogram, cardiac catheterization with pulmonary angiography; seven patients with CPE and eight with PPH had perfusion lung scans. Progressive dyspnoea was the main feature in all the patients; four out of nine with CPE and none of the ones with PPH had a previous history of thrombophlebitis. In all the patients the electrocardiogram, chest x-ray and echocardiogram showed signs of pulmonary hypertension, so that a clear distinction between the two groups was not possible. Cardiac catheterization showed pulmonary pressure values higher in patients with PPH as compared to the ones with CPE (systolic pressure 96 mmHg vs 70 mmHg, diastolic pressure 49 mmHg vs 31 mmHg, mean pressure 65 mmHg vs 45 mmHg). Pulmonary angiography in more than half of the patients with CPE showed a "cut off" of two or more lobar branches of the pulmonary arteries. In the patients with PPH pulmonary angiography showed a dilatation of the main pulmonary artery and a diffuse bilateral hypoperfusion. Perfusion lung scan in all the cases of CPE showed zonal perfusion defects, while in all cases of PPH, with the exception of one, it was largely normal. Venograms in the districts of the inferior vena cava demonstrated thrombosis in two out of six patients with CPE. Negative venograms were found in the five patients with PPH who had this investigation performed. One patient with CPE had a surgical embolectomy, the other eight had anticoagulant oral treatment. During the follow-up period three patients with CPE and five with PPH died within five years and within fifteen months respectively, of the diagnosis.(ABSTRACT TRUNCATED AT 400 WORDS)

[Management of serious pulmonary embolism].

In-hospital mortality is high when pulmonary embolism is complicated by hemodynamic instability and/or pulmonary hypertension. Death occurs frequently within the first hours after admission. This implies specific diagnostic and therapeutic management. Spiral CT seems to be an excellent diagnostic procedure in this setting. However, pulmonary angiography and perfusion lung scan can also be employed. Cardiac echography can help in the diagnosis and therapeutic decision making. Supportive therapy mainly includes correction of hypovolemia if present, a limited volume loading in other cases, and the use of dobutamine. Norepinephrine is the drug of choice when hypotension is present. Thrombolytic agents are indicated in case of hemodynamic instability. Modalities of administration and contra indications are currently well established. Surgical embolectomy should be performed in cases of uncontrolled shock, when thrombolysis is contra-indicated or uneffective.

[Major pulmonary embolism].

The diagnosis of major pulmonary embolism should be considered in case of acute respiratory distress, particularly when there is high thromboembolic risk. Although clinical symptoms are not specific, some are suggestive: syncope or dizziness with cyanosis and polypnoea, and especially arterial hypotension and cardiogenic shock. Diagnostic workup should be rapid and straight forward. Transthoracic echography is particularly useful to detect right heart thrombi and right ventricular overload. More information could be provided by helical computed tomography or perfusion lung scan or less commonly now by pulmonary angiography, depending on the patient's clinical condition and the available equipment. The mortality rate can reach 20 to 30%, and up to 65% after resuscitated cardiac arrest. Rapid desobstruction is justified through surgical embolectomy or intravenous thrombolysis favouring short duration protocols (alteplase over 2 h), in spite of the bleeding risk.

[A case of renal vein thrombosis and pulmonary embolism associated with diffuse membranous glomerulonephritis: the usefulness of low-molecular-weight heparin and urokinase therapy].

We report a case of renal vein thrombosis (RVT) and pulmonary embolism associated with diffuse membranous glomerulonephritis. A 44-year-old Japanese male was referred to the Nephrology Department with heavy proteinuria. Renal biopsy revealed diffuse membranous glomerulonephritis and we administered PSL 30mg/day and dipyridamole 300mg/day. Three weeks later, he was admitted with severe chest pain, dyspnea and massive proteinuria. RVT and pulmonary embolism were detected on CT scan and perfusion lung scan. After a few days of continuous intravenous unfractionated heparin (UFH) therapy, we used 72 U (anti-FXa)/kg of intravenous low-molecular-weight heparin (LMWH) every 12 hours for 10 days. He also received urokinase at the dose of 120,000 U/day for 4 weeks and long-term therapy with warfarin potassium at the dose of 3 mg/day. One month later, the thrombi in the pulmonary arteries and inferior vena cava disappeared on CT scan and perfusion lung scan. LMWHs have a longer biological half-life and a lower bleeding tendency than UFH for an equivalent antithrombotic effect. This case indicates that intermittent intravenous LMWH administration combined with urokinase is effective against RVT and pulmonary embolism without any side effect.

[Thrombolysis in pulmonary embolism - initial experience].

Pulmonary embolism (PE) is a clinical situation difficult to diagnose, at times of great clinical instability, above all when it is massive, which leads to difficulties in the approach and treatment of patients. The treatment has not had any major innovations in recent years, being conventional the use of heparin and more rarely embolectomy. Recently, some clinical trials have defended the use of thrombolytics. The objéctive of this paper is to present our experience, although the series is still small. From April 1996 to November 1997, 11 patients were admitted to our Cardiac Intensive Care Unit with the clinical suspicion of PE, 5 of which with great hemodynamic instability and suspicion of massive PE. The clinical presentation was sudden dyspnea and loss of consciousness in 2 patients, dyspnea and hypotension in 2 patients and shock and respiratory arrest in one case. Gasimetry revealed acute hypoxemia and hypocapnia in all cases, average partial blood pressure in O2 (pO2) of 59 mm Hg and CO2 (pCO2) of 19 mm Hg. ECC and thorax x-ray contributed to the diagnosis in 3 patients, transthoracic echocardiography was decisive for the diagnosis in 5 cases, with visualisation of the thrombus by transesophageal echocardiography in 3 patients. All patients were monitored by Swan-Ganz catheter, the average systolic pulmonary artery pressure (PAP) was 74 mm Hg. Thrombolysis with rTPA (10 mg bolus followed by 90 mg in perfusion in 2 hrs) was administered in 6 episodes in 5 patients. Only in the case of the patient in shock were other complications related to the use of thrombolytics namely high digestive hemorrhage. There was a clear clinical improvement in all cases with great relief of dyspnea reduction of cyanosis and jugular engurgitation. The patient in shock recovered systemic pressures and improved the hemodynamic state. A significant reduction in PAP was observed (average of 32.5 mm Hg). PE recurred in two cases: with one death and therapeutic thrombolytic was repeated in the other patient with good results. After discharge, all patients remained asymptomatic under oral anticoagulation. Despite this small series, the results favour the use of thrombolytics in PE with a clear clinical and hemodynamic improvement.

Pulmonary hypertension in patient with elevated homocystein level and blast injuries.

38-year-old man had chronic deep venous thrombosis (DVT) as a result of multiple injuries caused by an explosion of grenade 12 years ago, with recurrent pulmonary thromboembolisms and pulmonary hypertension which was unrecognized for a decade. Patient was admitted with a progressive dyspnea and exercise intolerance (NYHA II). The diagnosis was established according to clinical symptoms, transthoracic echocardiography, phlebography, lung scintigraphy and pulmonary angiography. Oral anticoagulant therapy was introduced and cava filter indicated to implant. During phlebography a floating thrombus was found in the inferior cava vein underneath renal vein. Implantation was delayed and patient received systemic fibrinolytic therapy with streptokinase (7500 000 UI within 4 days), followed by heparin infusion and warfarin. Post-fibrinolytic phlebography showed clear lumen of inferior vena cava. Fibrinolysis had also affected pulmonary hypertension-systolic pressure in the right ventricle measured by Doppler echocardiography decreased from 90 to 65 mmHg. Permanent intravenous cava filter was implanted.

[Low doses of rtPA administered as a bolus in treatment of clinically acute massive pulmonary embolism].

12 patients (7 male and 5 female) with confirmed pulmonary embolism (PE) with: angiography-5 cases, conventional contrast-enhanced CT-2 cases, echocardiography-2 cases, autopsy-3 cases were diagnosed as clinically acute PE. Criteria of clinically acute PE were: cardiac arrest-1 case-2 cases, shock-1 case, acute cor pulmonale-9 cases and acute cor pulmonale with shock. All patients were treated with heparin, administered with therapeutic prolongation of aPTT. Clinically acute PE (if possible confirmed with angiography, TC and/or echocardiography) was treated with rtPA administered in 10 minutes lasting bolus in doses 0.6-0.8 mg per kg of body weight (50 mg of rtPA during 10 minutes administered into peripheral veins). In 9 patients with pulmonary hypertension, significant decrease of tricuspidal gradient (measured echocardiographically during several hours after administration of rtPA) was documented. Improvement in PaO2, SaO2 and decrease of heart rate and respiratory rate were also achieved. No serious bleeding complications were observed after mentioned treatment. Control investigations (conventional contrast-enhanced CT and spiral CT) performed several days after rtPA administration revealed thrombus in pulmonary artery. We conclude: I rtPA administered in bolus simultaneously with heparin significantly decreased pulmonaryhypertension; rtPA administered simultaneously with heparin is safe method of treatment of PE; hemodynamic improvement after administration of rtPA is not univocal with full fibrynolitic effect.

Preoperative balloon pulmonary angioplasty enabled noncardiac surgery of a patient with chronic thromboembolic pulmonary hypertension (CTEPH): A case report.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease with a poor prognosis, characterized by chronic thromboembolic obstruction of the pulmonary arteries and pulmonary hypertension. Balloon pulmonary angioplasty (BPA) is a newly emergent treatment for CTEPH, which may substitute pulmonary endarterectomy, the standard but more invasive treatment for CTEPH. Here, we report the case of a CTEPH patient who underwent 2 noncardiac surgeries without complications after preoperative intervention of BPA. A 79-year-old man presented with severe osteoarthritis of bilateral knees, with adaptation of total knee arthroplasty (TKA). Transthoracic echocardiogram revealed severe pulmonary hypertension with estimated right ventricular systolic pressure of 140 mm Hg. Pulmonary arteriography revealed total occlusion of the upper branch of the right pulmonary artery, and ventilation/perfusion scan showed multiple mismatched perfusion defects. His pulmonary artery pressure (PAP) was as high as 89/25 (46) mm Hg with normal range of pulmonary capillary wedge pressure. He was diagnosed with CTEPH. Four BPA sessions for 8 branches of the bilateral pulmonary arteries were done, until the mean PAP (mPAP) went under 30 mm Hg. For the TKA, we selected spinal anesthesia in order to minimize intraoperative hemodynamic changes. Cardiac surgeons were standby in case extracorporeal membrane oxygenation (ECMO) initiation was required. With appropriate pain management and use of intravenous vasopressors, intraoperative vital signs were stable. No symptoms of hemodynamic collapse were observed postoperatively. The patient was discharged on the 46th postoperative day following rehabilitation. Two years later, left-side unicompartment knee arthroplasty (UKA) was scheduled. Right heart catheterization study revealed the mPAP was 30 mm Hg, nearly the same value as the last study. The operation was performed under spinal anesthesia with continuous arterial pressure monitoring without need for intraoperative vasopressor. He was discharged without complications on the 24th postoperative day. BPA can be an effective preoperative intervention for CTEPH patients undergoing noncardiac surgery.

[A case of pulmonary thromboembolism with pulmonary hypertension with marked improvement by oral PGI2 analogue].

The patient was a 71-year-old man with dyspnea and bilateral leg edema. He was admitted to our hospital with worsening of dyspnea and had received therapy for chronic heart failure in another hospital. On admission, chest X-ray film revealed dilatation of the cardiac silhouette (CTR: 58%). Electrocardiogram showed atrial fibrillation and negative T wave in II, III, and aVF. Cardiac arteriogram showed no organic lesions, but pulmonary hypertension, pulmonary artery pressure of 60/21/34 mmHg, right ventricular pressure of 40/9/20 mmHg were recognized in pulmonary hemodynamics. The diagnosis of chronic pulmonary thromboembolism was made on the basis of pulmonary arteriogram findings and multiple defects of lung perfusion scintigram. After administration of oral PGI2 analogue for one month, lung perfusion scintigram and right cardiac pressure were markedly improved.

[Characteristics of acute, hemodynamically stable pulmonary embolism presenting as a syncope].

Syncope (S) occurs in approximately 10% patients with acute pulmonary embolism (APE) and is commonly ascribed to the massive, hemodynamically instable APE. The aim of the study was to assess the occurrence and significance of S revealing hemodynamically stable APE. We found syncope in 6 of 21 (29%) consecutive patients (16 females, 5 males; age from 46-87 years, mean age of 71 years) who were diagnosed with APE and in whom other reasons for S were excluded. All patients were treated with anticoagulation. They all survived hospitalization and no APE recurrences were found during in-hospital period. Patients with APE-S compared to patients with APE and without S had smaller baseline RVED (21.2 +/- 2 vs. 27.3 +/- 5.6, p = 0.01), however both groups did not differ statistically in baseline vital signs, angiographic, hemodynamic, other echocardiographic parameters as well as in the results of laboratory findings. It is concluded, that S signals hemodynamically stable APE more frequently than is quoted. APE-S patients could not be clearly discriminate from APE patients without S on the basis of the parameters studied and S did not impact the course of APE during in- hospital period.

Development of a postoperative occlusive thrombus at the site of an implanted inferior vena cava filter: A case report.

Although an inferior vena cave (IVC) filter is placed to prevent fatal pulmonary embolism (PE), several complications associated with an IVC filter have been reported. We describe a case with symptomatic PE, of which the origin was an occlusive IVC thrombus that developed from the placement of an IVC filer after a laparoscopy-assisted total gastrectomy (LATG). A 71-year-old man underwent LATG under general anesthesia alone. He had an IVC filter implanted 13 years ago. An intravenous infusion of unfractionated heparin was substituted for the discontinuation of oral warfarin four days before the surgery. The proposed operation was performed and took a total of 404 minutes including the total duration of pneumoperitoneum that took 374 minutes. After the surgery, he experienced severe shivering reactions that required frequent bolus infusions of antihypertensive drugs. On the third postoperative day, he complained of dyspnea after taking a short walk, and subsequently lost consciousness. While he spontaneously recovered without requiring any resuscitation efforts, we performed computed tomography (CT) examination for suspected PE. The CT showed that a massive thrombus was occupying the intravenous space from the IVC filter to the left common iliac vein with several embolic defects in the peripheral pulmonary arteries present. An anticoagulant therapy was established with 10 mg of oral apixaban given twice a day for the first four days, followed by a reduction to 5 mg. On the 17th postoperative day, an ultrasound vascular examination confirmed the complete disappearance of deep venous thrombus (DVT). As an IVC filter itself may be a potential source of DVT, we should carefully manage patients with a previously implanted IVC filter throughout the perioperative period.

Acute pulmonary embolism. Aggressive therapy with anticoagulants and thrombolytics.

Patients with acute pulmonary embolism are at risk for early death or chronic morbidity. Appropriate therapy can dramatically reduce the incidence of both. Oxygen and heparin therapy should be started as soon as the diagnosis is suspected. The condition of a hypotensive patient with right ventricular overload from acute pulmonary embolism usually is made worse by a fluid challenge; hypotension may be relieved by preload reduction or even by gentle diuresis. Norepinephrine (Levophed), isoproterenol hydrochloride (Isuprel), and epinephrine are the pressor agents of choice. Immediate thrombolysis is the standard of care for any patient with significant hypoxemia or hypotension due to proven pulmonary embolism. Beyond this, the potential benefit of using thrombolytic agents should be considered routinely for every patient with proven pulmonary embolism. Surgical embolectomy is useful for unstable pulmonary embolism when there are absolute contraindications to thrombolysis or when thrombolytic therapy fails. Empirical use of thrombolysis may be considered as a last-ditch effort for a critically ill patient when there is a high clinical suspicion of pulmonary embolism. Standard closed-chest cardiopulmonary resuscitation is ineffective when the pulmonary circulation is obstructed by thrombus. Emergency thoracotomy or femorofemoral cardiopulmonary bypass is appropriately used in patients with full cardiac arrest from pulmonary embolism.

Management of mobile right heart thrombi: a prospective series.

Mobile right heart thrombi (MRHT) are uncommon but their true prevalence is unknown. The aim of our study was to assess the prevalence of MRHT by a systemic use of transthoracic echocardiography in a prospective series of consecutive patients admitted for acute severe pulmonary embolism (PE) and to adopt intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) as the first line intention to treat patients with proven MRHT. We performed a systematic transthoracic echocardiogram from November 1997 to June 1999 in 335 consecutive patients admitted for suspected acute massive PE in whom the diagnosis was subsequently confirmed by perfusion lung scan or angiography. MRHT was identified in 12 of the 335 patients (4%). Nine patients presented a coil form and three patients a ball form. The thrombolytic employed in all cases was rt-PA according to the following protocol: 10 mg in a bolus and 40 mg over 2 h, followed by 50 mg over 5 h, up in a total dose of 100 mg, associated with a bolus of 5000 units of heparin. Control echocardiograms were performed 12 h after the initiation of treatment and at 12-month follow-up. Three patients died before the onset of thrombolytic infusion. The nine remaining patients were submitted to thrombolytic therapy using rt-PA. In seven of the nine remaining patients, MRHT was no longer observed after 12 h and the echocardiographic signs of RV overload had disappeared. The two last patients required adjunctive surgery because of evidence of persistent thrombus in a pulmonary artery. After 24 h, both scintigraphy and angiography demonstrated improved pulmonary perfusion. At 1-year follow-up, all patients were alive and the pulmonary artery pressure estimated by Doppler echocardiography was <30 mm Hg. The incidence of right heart thrombus is low in patients admitted for acute PE. Thrombolytic therapy with rt-PA appears to be rapidly effective in most patients with MRHT. The thrombus usually resolves and pulmonary perfusion is rapidly improved. Systematic echocardiogram appears to be useful for rapidly detecting MRHT in patients with suspected massive PE.

Pulmonary embolectomy in a case of subacute pulmonary embolism, with previous unsuccessful fibrinolysis

Pulmonary embolism is a potentially fatal heart condition that requires prompt restoration of blood flow in the pulmonary vascular bed and prevention of recurrent events. Mortality is associated to the degree of hemodynamic repercussion, complications and opportunity in the treatment. Male 33 years of age who began with sudden dyspnea, chest pain of moderate intensity, sweating and syncope. His admission vitals signs: blood pressure 100/70 mm Hg, heart rate 125 beats per minute, respiratory rate 24; peripheral saturation 85 %. Physical examination: grade I jugular engorgement at 45 degrees, rhythmic heart sounds, with auscultation of systolic murmur I/IV in tricuspid focus and second reinforced heart sound. Rest of exploration without relevant data. The echocardiogram showed data of right ventricular failure and systolic pulmonary artery pressure of 60 mm Hg; the angiotomography showed thrombosis of both branches of the pulmonary artery. The patient received fibrinolytic therapy with tecneteplase 50 mg single bolus and antithrombotic therapy. Due to persistence of residual thrombus, the patient underwent surgical bilateral embolectomy. Surgical pulmonary embolectomy rescue is an alternative management with highly satisfactory results.

Dasatinib-Induced Pulmonary Arterial Hypertension Treated with Upfront Combination Therapy.

Pulmonary arterial hypertension (PAH) is a rare complication of dasatinib that was approved as a first-line therapy for chronic myelocytic leukemia (CML). A 24-year-old man presenting dyspnea at rest and leg edema was admitted to our hospital. He had been diagnosed with CML and prescribed dasatinib for 4 years. Chest X-ray showed significant bilateral pleural effusion and heart enlargement. Echocardiography revealed interventricular septal compression and elevated peak tricuspid regurgitation pressure gradient of 66.7 mmHg indicating severe pulmonary hypertension. After the other specific diseases to provoke PAH were excluded, he was diagnosed with dasatinib-induced PAH. Despite discontinuation of dasatinib and intravenous administration of diuretic for two weeks, World Health Organization (WHO) functional class was still II and mean pulmonary arterial pressure (PAP) was high at 37 mmHg. Therefore, we administered sildenafil and bosentan together as an upfront combination therapy three weeks after dasatinib discontinuation. Six months later, his symptoms improved to WHO functional class I and mean PAP was decreased to 31 mmHg. Although PAH is a rare complication of dasatinib, symptomatic patients prescribed with dasatinib should have an echocardiogram for PAH screening. Moreover, the upfront combination therapy would be a useful option for symptomatic patients after discontinuation of dasatinib.

[Therapy of acute pulmonary thromboembolism from the physician's standpoint].

The therapy of acute pulmonary thromboembolism (APTE) is based on the clinical grade and ranges from ambulant therapy with anticoagulation, to thrombolysis, inferior vena cava (IVC) filtration, and catheter thrombectomy. In the absence of contraindications, initial treatment of APTE should consist of parenteral anticoagulation with unfractionated heparin. Long-term anticoagulation therapy, usually with warfarin, should be administered according to the individual risk profile of the patient. Thrombolytic therapy may be appropriate for patients with massive APTE with cardiac shock, syncope, etc. Similarly, thrombolysis has been reported to be effective in submassive APTE with right ventricular overload on echocardiography. IVC filters should be reserved for APTE with deep vein thrombosis (DVT) in which there are absolute contraindications to anticoagulation, recurrent thromboemboli despite therapeutic anticoagulation, and status after surgical thrombectomy. Relative indications for IVC filters that require individualized decision making include proximal DVT, especially with free-floating thrombi or in patients with limited cardiopulmonary reserve. For patients with massive APTE with contraindications to anticoagulation or in whom anticoagulation is uneffective, transcatheter aspiration with catheterization or fragmentation using a guidewire and rotating pig-tail catheter can be used. In addition, cardiopulmonary management such as supplemental oxygen, catecholamine administration, percutaneous cardiopulmonary support, etc. may be necessary for individual patients.

Pulmonary hypertension

Exclude other diseases If the echocardiogram is compatible with a diagnosis of pulmonary hypertension, common causes of pulmonary hypertension (left heart disease and lung disease) are considered and further tests are performed accordingly. These tests generally include electrocardiography (ECG), pulmonary function tests including lung diffusion capacity for carbon monoxide and arterial blood gas measurements, X-rays of the chest and high-resolution computed tomography (CT) scanning. Ventilation/perfusion scintigraphy If heart disease and lung disease have been excluded, a ventilation/perfusion scan is performed to rule out CTEPH. If unmatched perfusion defects are found, further evaluation by CT pulmonary angiography, right heart catheterization, and selective pulmonary angiography is performed. CT scan

[Results of embolectomy in massive pulmonary embolism (author's transl)].

In ten patients successful embolectomy after acute massive pulmonary embolism was performed. Clinical symptoms included circulatory arrest and shock as well as collaps, syncope and dyspnoe. Pulmonary angiography regularly showed massive, bilateral emboli. In 9 patients more than one half of the pulmonary artery system was involved (perfusion defect more than 50%). Right heart catheterization demonstrated pulmonary hypertension in all cases. In 8 patients the pulmonary artery mean pressure (PAm) exceeded 30 mm Hg. In 9 patients there were signs of right heart failure (RVEDP more than 11 mm Hg). At recatheterization 6 to 30 (mean 19) days after operation using cardiopulmonary bypass there was a marked improvement of pulmonary angiograms, which were normal in 3 cases. PAm decreased from 34.3 mm Hg to 14.6 mm Hg postoperatively and RVEDP from 14.4 to 5.1 mm Hg (p less than 0.001). These results confirm, that pulmonary embolectomy leads to a good functional results.

[Successful operative case of chronic thromboembolic pulmonary hypertension clinically diagnosed as bronchial asthma].

We report a case of a 70-year-old man with chronic thromboembolic pulmonary hypertension (CTEPH) in whom bronchial asthma had been clinically diagnosed and treated, and who showed remarkable improvement by pulmonary endarterectomy. He had dyspnea on exertion and had been clinically treated for bronchial asthma for 15 years. However, his symptoms did not improve after oral and inhaled corticosteroid therapy, and he had dyspnea at rest. CTEPH was suspected by echocardiography and computed tomography (CT) and he was admitted to our hospital. Perfusion scans showed multiple segmental perfusion defects with normal ventilation study, and contrast-enhanced CT showed intramural thrombi in both pulmonary arteries. Right cardiac catheterization revealed a mean pulmonary arterial pressure of 70 mm Hg and pulmonary vascular resistance of 1699 dyn.s.cm(-5) with chronic thromboembolic findings on pulmonary angiography. After surgery his pulmonary hemodynamics and symptoms significantly improved. CTEPH is rarely diagnosed at the initial visit because the only symptom is dyspnea on exertion, and it is often misdiagnosed as other respiratory diseases. But it is important to suspect and diagnose CTEPH in patients with unexplained dyspnea because this disease can be cured by surgery.

[Repeated prolonged thrombolytic therapy after unsuccessful thrombolysis in massive pulmonary embolism: a case report].

We report on a 43-year-old woman who presented with shortness of breath and syncope due to massive pulmonary embolism. Transthoracic echocardiography showed signs of right ventricular overload, and contrast-enhanced chest computed tomography demonstrated filling defects in both main pulmonary arteries consistent with obstructing thrombi. Initially, thrombolytic therapy with recombinant tissue plasminogen activator was given, but shock was not resolved. Thrombolytic therapy was repeated with streptokinase and infusion was extended to 48 hours, which yielded a successful result without any hemorrhagic complication. Repeated prolonged thrombolytic therapy after initial unsuccessful thrombolysis can be considered an alternative option in massive pulmonary embolism.


The patient probably presents with bronchiolitis. At this stage, no additional tests should be performed unless there is a clinical worsening.

6-month-old infant presenting to the emergency department for respiratory distress. Examination: axillary temperature 37.2°C, respiratory rate 40 rpm, heart rate 160 bpm, blood pressure 90/45 mmHg, SatO2 95% on room air. He shows moderate respiratory distress with intercostal and subcostal retraction. Pulmonary auscultation: scattered expiratory rhonchi, elongated expiration and slight decrease in air entry in both lung fields. Cardiac auscultation: no murmurs. It is decided to keep the patient under observation in the hospital for a few hours. What do you consider the most appropriate attitude at this time with regard to the complementary tests?

Request venous blood gas, leukocyte count and acute phase reactants.

Request arterial blood gases and acute phase reactants.

Acute bronchitis

A variety of tests may be performed in people presenting with cough and shortness of breath: A chest X-ray is useful to exclude pneumonia which is more common in those with a fever, fast heart rate, fast respiratory rate, or who are old. A sputum sample showing neutrophil granulocytes (inflammatory white blood cells) and culture showing that has pathogenic microorganisms such as Streptococcus species. A blood test would indicate inflammation (as indicated by a raised white blood cell count and elevated C-reactive protein). Decreased breath sounds, crackles, wheezing, and rhonchi that clears with coughs may be heard in the chest. Dullness to percussion and pleural rub suggest disease extension beyond the bronchi such as seen with pneumonia. Paroxysms of cough followed by inspiratory whoop and vomiting suggests pertussis.

Clinical and Laboratory Findings in Patients With Acute Respiratory Symptoms That Suggest the Necessity of Chest X-ray for Community-Acquired Pneumonia.

Pneumonia is a common illness in all parts of the world and is considered as a major cause of death among all age groups. Nevertheless, only about 5% of patients referring to their primary care physicians with acute respiratory symptoms will develop pneumonia. This study was performed to derive practical criteria for performing chest radiographs for the evaluation of community-acquired pneumonia (CAP). A total of 420 patients with acute respiratory symptoms and positive findings on chest radiograph were evaluated from December 2008 to December 2009. The subjects were referred to outpatient clinics or emergency departments of Birjand's medical university hospitals, Iran, and were enrolled as positive cases. A checklist was completed for each patient including their demographic information, clinical signs and symptoms (cough, sputum production, dyspnea, chest pain, fever, tachycardia, and tachypnea), abnormal findings in pulmonary auscultation and laboratory findings (erythrocyte sedimentation rate, C-reactive protein levels, and white blood cell count). An equal number of age-matched individuals with acute respiratory symptoms, but insignificant findings on chest radiography, were included as the control group. Finally, the diagnostic values of different findings were compared. The data showed that vital signs and physical examination findings are useful screening parameters for predicting chest radiograph findings in outpatient settings. Therefore, by implementing a prediction rule, we would be able to determine which patients would benefit from a chest X-Ray (sensitivity, 94% and specificity, 57%). This study's findings suggest that requesting chest radiographs might not be necessary in patients with acute respiratory symptoms unless the vital signs and/or physical examination findings are abnormal. Considering the 94% sensitivity of this rule for predicting CAP, a chest radiograph is required for patients with unreliable follow-ups or moderate to high likelihood of morbidity if CAP is not initially detected.

Pulmonary examination

The pulmonary examination or respiratory examination is the portion of the physical examination where the physician examines the respiratory system for signs of disease. It is performed as a part of a complete physical examination, or the physician may choose to perform a focused respiratory exam. Classically, it is performed after the HEENT examination, and consists of four stages: inspection, palpation, percussion, and auscultation. If there are signs of respiratory disease, the physician may order additional tests including medical imaging, such as a chest X-ray or CT scan, or laboratory tests, such as a complete blood count. The information gathered from the physical examination, along with the medical history, is synthesized in order to produce a differential diagnosis and treatment plan. References Medical treatments

List of medical tests

medical test is a medical procedure performed to detect, diagnose, or monitor diseases, disease processes, susceptibility, or to determine a course of treatment. The tests are classified by speciality field allowing to know in which ward of hospital or by which specialist doctor are usually these tests performed. This list is not exhaustive but might be useful as a guide. Where available, ICD-10 codes are listed. Consulting Room Tests These tests are usually performed in a consulting room by any doctor and require no advanced equipment. general Temperature measurement, with a thermometer Patient's Respiratory rate measurement Blood oxygen concentration measurement taking the patient's pulse weighing, and measuring height and girth measuring blood pressure specific: abdominal palpation cardiac ausculation HEENT examination digital rectal examination neurological examination psychiatric assessment pulmonary auscultation vaginal examination

Community-acquired pneumonia

Hospitalization Some CAP patients require intensive care, with clinical prediction rules such as the pneumonia severity index and CURB-65 guiding the decision whether or not to hospitalize. Factors increasing the need for hospitalization include: Age greater than 65 Underlying chronic illnesses Respiratory rate greater than 30 per minute Systolic blood pressure less than 90 mmHg Heart rate greater than 125 per minute Temperature below 35 or over 40 °C Confusion Evidence of infection outside the lung Laboratory results indicating hospitalization include: Arterial oxygen tension less than 60 mm Hg Carbon dioxide over 50 mmHg or pH under 7.35 while breathing room air Hematocrit under 30 percent Creatinine over 1.2 mg/dl or blood urea nitrogen over 20 mg/dl White-blood-cell count under 4 × 10^9/L or over 30 × 10^9/L Neutrophil count under 1 x 10^9/L

Acute chest syndrome

Diagnosis The diagnosis of acute chest syndrome is made difficult by its similarity in presentation with pneumonia. Both may present with a new opacification of the lung on chest x-ray. The presence of fevers, low oxygen levels in the blood, increased respiratory rate, chest pain, and cough are also common in acute chest syndrome. Diagnostic workup includes chest x-ray, complete cell count, reticulocyte count, ECG, and blood and sputum cultures. Patients may also require additional blood tests or imaging (e.g. a CT scan) to exclude a heart attack or other pulmonary pathology. Prevention Hydroxyurea is a medication that can help to prevent acute chest syndrome. It may cause a low white blood cell count, which can predispose the person to some types of infection. Treatment Broad spectrum antibiotics to cover common infections such as Streptococcus pneumoniae and mycoplasma, pain control, and blood transfusion. Acute chest syndrome is an indication for exchange transfusion.

[A case of miliary tuberculosis associated with acute respiratory failure during pregnancy].

A case of miliary tuberculosis associated with acute respiratory failure during pregnancy was reported. A 39-year-old, 29-week pregnant woman was admitted to our hospital with complaints of nonproductive cough and fever on June 12. On admission, her temperature was 38.2 degrees C; pulse rate was 90/min., and blood pressure was 120/76 mmHg. Physical examination revealed moist rales at right lung basis. Chest X-ray showed small nodular infiltrates in right lower lung field. Laboratory data revealed positive CRP, accelerated ESR and increased level of alpha 2-globulin. The number of T-cells was markedly decreased (14/mm3). The PPD skin test was negative, and the sputum smears for acid-fast bacilli were negative. Suspected of bacterial or viral pneumonia, the patient was treated with antibiotics (CPM, EM and CAZ), which had no effects for her. On June 16, the Chest X-ray showed infiltrates throughout bilateral lung fields, and the patient became increasingly dyspneic. On June 18, the results of arterial blood gas, analysis under room air were: PaO2 26.7 Torr, PaCO2 29.0 Torr, pH 7.505. Because of severe hypoxemia, she was intubated and placed on a volume-cycled respirator. Hydrocortisone (1000 mg, daily) was added to treatment because ARDS was suspected. Since the smears of tracheobronchial secretions showed acid-fast bacilli on June 24, she was diagnosed to have miliary tuberculosis. Then the intensive therapy with antituberculosis drugs (isoniazid 400 mg, rifampicin 450 mg, and streptomycin 1g, daily) was started. The non specific antibiotics were discontinued; hydrocortisone was tapered and stopped. The next week, she became afebrile and hypoxemia steadily improved.(ABSTRACT TRUNCATED AT 250 WORDS)

Pneumonia

Physical exam Physical examination may sometimes reveal low blood pressure, high heart rate, or low oxygen saturation. The respiratory rate may be faster than normal, and this may occur a day or two before other signs. Examination of the chest may be normal, but it may show decreased expansion on the affected side. Harsh breath sounds from the larger airways that are transmitted through the inflamed lung are termed bronchial breathing and are heard on auscultation with a stethoscope. Crackles (rales) may be heard over the affected area during inspiration. Percussion may be dulled over the affected lung, and increased, rather than decreased, vocal resonance distinguishes pneumonia from a pleural effusion. Imaging

A 24-Year-Old Man With Dyspnea and a Broken Left Femur.

A 24-year-old White man presented with 1-day complaints of progressive shortness of breath and fever. He recently underwent an open reduction and internal fixation of a left midshaft femur fracture from a skiing accident 4 days ago. He denied chest pain, skin rashes, hemoptysis, hematemesis, melena, or surgical site bleeding. On arrival, the patient appeared in mild respiratory distress with a respiratory rate of 23 breaths/min, temperature of 37.8°C, heart rate of 97 beats/min, BP of 95/54 mm Hg, and peripheral saturation of 97% on 6-L/min nasal canula. His initial peripheral saturation on room air was 67%. Physical examination was unremarkable, except for diffuse rhonchi on chest auscultation. Chest radiograph on admission showed alveolar opacities predominantly in bilateral lower lobes. A chest CT angiography revealed no evidence for pulmonary embolism. However, there were findings of diffuse bilateral ground-glass opacities with areas of patchy consolidation and innumerous micronodules in both lungs (Fig 1). Laboratory examination was significant for a drop of hemoglobin by 3 g/dL and hematocrit level by 7% since his hospital discharge 4 days earlier. His renal function and urine analysis were normal. Venous blood gas on admission showed pH of 7.39 and Pco<sub2</sub of 43 mm Hg. Because of unexplained acute anemia, nonspecific CT chest findings and progressive dyspnea, a bronchoscopy with BAL was performed. Four aliquots of 60 mL saline solution were injected for lavage with fluid return (Fig 2). BAL fluid showed WBC count of 0.411 × 10<sup3</sup/mm<sup3</sup, RBC count of 318 × 10<sup3</sup/mm<sup3</sup, 100% fresh RBCs, 73% neutrophil, 24% lymphocytes, 1% monocytes, and 2% eosinophils. BAL fluid cytologic condition is shown in Figure 3. A full vasculitis workup by rheumatology was unremarkable. Ophthalmologic and skin examination were unrevealing.

Diagnostic value of lung auscultation in an emergency room setting.

In daily routine, physicians use history, physical examination and technology-based information such as laboratory tests and imaging studies to diagnose the patients' disease. We determined the diagnostic value of lung auscultation in patients admitted to the Medical emergency room with chest symptoms. Two-hundred-and forty-three consecutive patients (137 males), mean age 59.2 years were included. Internal Medicine registrars had to make a presumptive diagnosis, 1) after having taken the history and 2) after having auscultated the lungs. Thereafter, routine diagnostic procedures were performed. The estimated diagnosis was compared with the final diagnosis based on the written report to the Family Practitioner. Two-hundred-eighty-seven diagnoses were made. Eighteen percent of patients suffered from left heart failure, 13% from unexplained chest pain, 10.5% from chest wall pain, and 10.5% from pneumonia. Forty-one percent of the diagnoses were already correct when based only on the patient's history. Lung auscultation improved the diagnostic yield only in 1% and worsened it in another 3%. By multiple logistic regression, normal lung auscultation (OR 0.12 [95CI% 0.053-0.29]) was the independent predictor for not having a lung or heart disease. However, elevation of B-type natiuretic peptide (BNP) (OR 1.16 per 100 pg/ml (95CI% 1.004-1.35), wheezing (OR 0.023 [0.002-0.33]) and pCO2 (OR 0.25 (0.10-0.621) were independent predictors for having a heart disease, whereas wheezing (OR 7.41 [3.26-16.83]) and CRP (OR 1.008 per 10 units [1.003-1.014]) were risk factors for having a lung disease. In contrast to history taking, abnormal lung auscultation does not appear to contribute considerably to the final diagnosis in patients presenting with chest symptoms in an emergency room setting. However, normal lung auscultation is a valuable predictor for not having a lung or heart disease, whereas wheezing is a predictor for having a lung disease and not having a heart disease.

Myocardial infarction diagnosis

Physical examination The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38–39 °C). Blood pressure may be elevated or decreased, and the pulse can become irregular. If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation, such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung. Electrocardiogram

[Fulminant, life-threatening influenza A/H1N1 virus infection].

A 52-year-old man presented with unproductive cough, fever and chill in our emergency department. Self-medication with amoxicillin over 3 days failed to improve his condition. The patient was in poor general condition. His body temperature was 38.4 C, with a heart rate of 124/min, a blood pressure of 120/70 mmHg and a positive shock index. At auscultation of the chest fine rales were heard over both lungs with diminished percussion sounds basal. The respiratory rate was 30/min and the oxygen saturation of 84% at room air. Laboratory: signs of inflammation; blood gas analysis: pronounced hypoxemia. A chest radiogram revealed signs of extensive pulmonary infiltrates on both sides. The patient was admitted to our Intensive Care Unit. He received piperacillin, sulbactam and levoflaxacin, ample fluid and non-invasive ventilation as well as intermittent catecholamine treatment. As there was no clinical improvement the patient was intubated on day 3. On bronchoscopy viral etiology was suspected. At this time the respiratory situation deteriorated. Acute respiratory distress syndrome (ARDS) was diagnosed. An antifungal and antiviral treatment (voriconazol, oseltamivir) was started and a cortisone pulse was attempted. The patient was transferred to another clinic where extracorporeal membranoxygenation (ECMO) was performed on the same day. The following day influenza A/H1N1-test was confirmed. Ten days after transfer, the patient regained spontaneous respiration, and he most likely survives the infection. The incidence of influenza (A/H1N1) has increased in Germany and severe and lethal courses have occurred. Therefore, the diagnostic and treatment algorithms need to be reconsidered in order to rapidly diagnose and treat infections.

The spectrum of patients strongly influences the usefulness of diagnostic tests for pneumonia.

To study the influence of the spectrum of patients on the usefulness of five clinical cues, "very annoying dyspnoea", "strong lateral chest pain", crackles, C-reactive protein analysis, and erythrocyte sedimentation rate in the diagnosis of pneumonia. Evaluating the diagnostic properties of the cues against radiographic pneumonia at four steps in the diagnostic process, associated with increasing prevalence of pneumonia: 1. in all the 581 patients included, 2. in 402 of these patients who underwent physical chest examination, 3. in 188 patients classified by the doctors as having a lower respiratory tract infection, and 4. in 79 patients referred for radiography by the doctors. The municipal emergency clinic in Tromsø, Norway. 581 adult patients with respiratory tract infection. Sensitivity, specificity, Likelihood Ratio, and Positive predictive value. A tendency of decreasing specificity and Likelihood Ratio with increasing prevalence of pneumonia was demonstrated for all test, except for C-reactive protein analysis. This tendency may be explained either by the emphasis laid on the tests by the doctors when selecting patients for the diagnostic steps, or by an association between the evaluated tests and those emphasized by the doctors. As the diagnostic value of symptoms and signs are strongly influenced by selection, caution should be shown when transferring diagnostic values from one clinical setting to another.

Acute respiratory distress syndrome

According to the 2012 Berlin definition, adult ARDS is characterized by the following: lung injury of acute onset, within 1 week of an apparent clinical insult and with the progression of respiratory symptoms bilateral opacities on chest imaging (chest radiograph or CT) not explained by other lung pathology (e.g. effusion, lobar/lung collapse, or nodules) respiratory failure not explained by heart failure or volume overload decreased Pa/Fi ratio (a decreased Pa/Fi ratio indicates reduced arterial oxygenation from the available inhaled gas): mild ARDS: 201 – 300 mmHg (≤ 39.9 kPa) moderate ARDS: 101 – 200 mmHg (≤ 26.6 kPa) severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa) Note that the Berlin definition requires a minimum positive end expiratory pressure (PEEP) of 5 cm for consideration of the Pa/Fi ratio. This degree of PEEP may be delivered noninvasively with CPAP to diagnose mild ARDS.

[How much pulmonary diagnostics does the family physician need?].

Spirometry plays the major role in pulmonary diagnostics in the family practice, but is still used much too rarely on patients with respiratory symptoms. Every patient with shortness of breath or a chronic, persistent cough should have spirometry performed. Needless to say, taking a selective medical history and auscultation of the lungs and heart are additional, important pillars for making a diagnosis. Measurement of the peak expiratory flow (PEF) can be especially helpful in emergencies. Pulse oxymetry also aids in the assessment of acute situations and additionally, can provide valuable information in the follow-up treatment of chronic respiratory diseases.

Acute respiratory distress in a silversmith.

A 25-year-old young male patient presented in casualty department with severe respiratory distress on the fourth day from onset of symptoms. The patient was nonsmoker and had no antecedent medical or drug history. Prior to admission, patient had dry cough and bilateral pleuritic chest pain for the last three days. He was in severe respiratory distress with use of accessory muscles of respiration. On examination, he had heart rate of 120 beats/min, blood pressure (BP) of 150/80, respiratory rate of 48-52/min and central cyanosis present. On systemic examination, reduced intensity of breath sounds with extensive rhonchi and crepitation was found in both lung fields, with other examination being within normal limits. On pulse oximetry, oxygen saturation was 28% on room air, which increased up to 36% with the help of 4 L oxygen via nasal prongs. PaO2/FiO2 ratio was 100. Chest X-ray analysis was suggestive of non-cardiac pulmonary edema in view of bilateral fluffy opacity without cardiomegaly. In view of 2/3 positive criteria, his provisional diagnosis was Acute Respiratory Distress Syndrome (ARDS). He required mechanical ventilatory support and was gradually weaned over a period of 10 days. The patient was treated with broad spectrum antibiotics and other supportive measures. On re-evaluation of history, we found that he was a goldsmith by occupation, smelting silver and gold for the past 8-10 years. On the day of onset of symptoms, while smelting silver he was exposed to golden yellow fumes for around 15 minutes, with the quantum of exposure more than any other day earlier. From previous experience and analysis of similar silver metals, he was able to tell us that the silver was adulterated with large amount of cadmium on that day than before. Serum level of cadmium was 2.9 μg/L 6 days after initial exposure. At the time of discharge, he had residual opacities in the chest radiograph and resting oxygen saturation was 94% on room air.

[Lung auscultation--an overview].

The auscultation of the lungs is - among anamnesis - the most important part in the assessment of patients presenting with pulmonary symptoms. The lung auscultation is reproducible, cost efficient and very helpful to distinguish between differential diagnoses, in particular in emergency situations. Detection and description of lung sounds requires experience and should be performed by strict adherence to the internationally accepted terminology.

Air embolism

Venous or pulmonary air embolism occurs when air enters the systemic veins and is transported to the right side of the heart and from there into the pulmonary arteries, where it may lodge, blocking or reducing blood flow. Gas in the venous circulation can cause cardiac problems by obstructing the pulmonary circulation or forming an air-lock which raises central venous pressure and reduces pulmonary and systemic arterial pressures. Experiments on animals show that the amount of gas necessary for this to happen is quite variable. Human case reports suggest that injecting more than 100 mL of air into the venous system at rates greater than 100 mL/s can be fatal. Very large and symptomatic amounts of venous air emboli may also occur in rapid decompression in severe diving or decompression accidents, where they may interfere with circulation in the lungs and result in respiratory distress and hypoxia.

Counting respiratory rate in infants under 2 months: comparison between observation and auscultation.

The World Health Organization's global programme for the control of acute respiratory infections relies on counting respiratory rate (RR) by observing abdominal and chest movements in order to diagnose pneumonia. However, few studies on the reliability of the observation method have been published. We counted RR simultaneously by observation and auscultation in 100 healthy infants at 1, 2, 4, 6 and 8 weeks of age for 15, 30 and 60 sec, and compared RRs obtained by the two methods. In all the age groups studied, the co-efficients of variation for the RRs recorded by observation or auscultation were similar. The mean RR by observation was higher by 1-3 breaths/min than mean RR by auscultation (p < 0.001). The 95% confidence interval (+/-2 SD) for the difference between RR by the two methods ranged from +5 to -8 breaths/min for RR counted for 1 full minute. Our data support the assumption that observation is as reliable as auscultation for counting RR.

Lung injury from inhaling butane hash oil mimics pneumonia.

"Dabbing", a relatively new form of THC use which utilizes Butane Hash Oil (BHO), an extraction of dried cannabis containing high levels of butane and terpene byproducts. The extraction process yields a waxy substance that is heated, vaporized and inhaled. We describe a lung injury as a result of BHO use. A previously healthy 18-year-old female presented to the ED with shortness of breath for 3-4 days. Initial oxygen saturation was 79% on room air. She was refractory to bronchodilators, steroids and supplemental O<sub2</sub. She has a 1-pack year smoking history and daily BHO abuse. Chest x-ray was positive for bilateral patchy infiltrates with mild hyperinflation. CT was negative for Pulmonary Embolus or other acute pathologic process. Sputum gram stain and blood cultures were negative. Arterial blood gases confirmed a pO2 of 73 mmHg. On physical exam she was tachycardic and tachypneic. Respiratory auscultation showed decreased air entry bilaterally with diffuse expiratory wheezing, bilateral rhonchi and a prolonged expiratory phase. We concluded her severe pneumonitis was secondary to daily BHO inhalation. Heating BHO to high temperatures, releases up to 75% of THC, compared to 5-20% THC in traditional smoked cannabis. At 978°F terpenes degrade into methacrolein and benzene. Methacrolein is structurally similar to acrolein, a pulmonary irritant, which causes acute lung injury and pulmonary edema in laboratory animals. We hypothesize a mechanism of lung injury and acute respiratory failure secondary to inhalation of high levels of methacrolein and benzene related to relatively novel phenomena of BHO use.

[Lung auscultation in the 21th century].

Lung auscultation is an essential part of the physical examination for diagnosing respiratory diseases. The terminology standardization for lung sounds, in addition to advances in their analysis through new technologies, have improved the use of this technique. However, traditional auscultation has been questioned due to the limited concordance among health professionals. Despite the revolu tionary use of new diagnostic tools of imaging and lung function tests allowing diagnostic accuracy in respiratory diseases, no technology can replace lung auscultation to guide the diagnostic process. Lung auscultation allows identifying those patients who may benefit from a specific test. Moreover, this technique can be performed many times to make clinical decisions, and often with no need for- complicated and sometimes unavailable tests. This review describes the current state-of-the-art of lung auscultation and its efficacy based on the current respiratory sound terminology. In addition, it describes the main evidence on respiratory sound concordance studies among health professionals and its objective analysis through new technology.

Respiratory sounds

Other tests of auscultation

Sepsis

The Surviving Sepsis Campaign has recommended 30 ml/kg of fluid to be given in adults in the first three hours followed by fluid titration according to blood pressure, urine output, respiratory rate, and oxygen saturation with a target mean arterial pressure (MAP) of 65 mmHg. In children an initial amount of 20 ml/kg is reasonable in shock. In cases of severe sepsis and septic shock where a central venous catheter is used to measure blood pressures dynamically, fluids should be administered until the central venous pressure reaches 8–12 mmHg. Once these goals are met, the central venous oxygen saturation (ScvO2), i.e., the oxygen saturation of venous blood as it returns to the heart as measured at the vena cava, is optimized. If the ScvO2 is less than 70%, blood may be given to reach a hemoglobin of 10 g/dL and then inotropes are added until the ScvO2 is optimized. In those with acute respiratory distress syndrome (ARDS) and sufficient tissue blood fluid, more fluids should be given

[Auscultation of the lungs--still a useful examination?].

Auscultation of the lungs has been a central element in clinical examination since the early part of the nineteenth century. However, the role of the stethoscope in our diagnostic work-up has more and more been challenged by newer diagnostic equipment. Research carried out over the last 30 years has given us new knowledge about the physical basis of lung sounds and the meaning of the sounds. Electronic stethoscopes and computer-based analysis of digital lung sounds are now available. Lungs auscultation findings should be interpreted with caution and be related to the case history and other clinical findings.

The diagnosis of adult pneumonia in general practice. The diagnostic value of history, physical examination and some blood tests.

Because of lower respiratory infection that was treated with antibiotics on the suspicion of pneumonia, 71 patients aged 15 years or more were referred to the study by general practitioners. Using a positive chest X-ray as a "gold standard", 15% had pneumonia. The diagnostic value of variables from history, physical examination and blood tests was evaluated by calculating the likelihood ratio (LR). A duration of illness less than 24 hours before consulting the general practitioner was the variable from the history with the highest LR, 13.5. The white blood cell count and particularly the C-reactive protein analysis had a high diagnostic value, CRP greater than 50 mg/l had an LR of 37. In this selected material pulmonary symptoms and lung findings were of minor value in differentiating patients with and without pneumonia, with no LR exceeding 2.3. This can be explained to some extent by selection bias.

Report of a lung carcinoma extended to the left atrium through pulmonary vein.

Lung cancers may extend along or grow through the pulmonary veins to invade or lie within the left atrium (LA). A 62-year-old man, previously healthy, presented with 1-month ventilatory-independent right hemithorax back pain, dry cough and large effort dyspnea. He also referred weight loss of 12 kg in 10 months and denied hemoptysis. As antecedents, he smoked for 40 years and moderate daily alcoholism. On physical examination, the patient was in good general condition, hydrated and regular respiration at rest [blood pressure (BP) =120/80 mmHg; heart rate (HR) =90 bpm; respiratory rate (RR) =16 rpm]. Cardiac auscultation revealed two standard rhythmic sounds without murmurs. Pulmonary auscultation revealed a slightly diminished vesicular murmur in the lower 1/3 of the right hemithorax without adventitious noises. Chest radiography showed a mass over the right lower lung. A CT scan confirmed the radiography image with the mass extending along the right inferior pulmonary vein and a tumor in the LA. Transthoracic and transesophageal echocardiography revealed large mass within the LA (occupying almost the entire cavity), measuring about 10 cm × 3 cm at its largest diameter, prolapsing into the left ventricle. Bronchoscopy, head CT scan, and whole-body bone scintigraphy investigation did not show any distant metastasis. The patient was successfully operated removing the intracardiac and inferior pulmonary vein tumor with the aid of cardiopulmonary bypass, followed by a right inferior lobectomy carried out after 25 days. After 30 days from surgery presented seizures associated a brain metastasis evidenced by CT when adjuvant radio and chemotherapy was started. During the next 90 days, the clinical conditions worsened, and the patient died 4 months after the surgical treatment. The case report has two primary justifications, even considering the poor outcome: (I) rarity and (II) the possibility of the surgical treatment.

The lung exam.

Accurate diagnosis is essential for effective treatment. After history-taking, the physical examination is second in importance in assessing a pulmonary patient. The time-honored sequence of inspection, palpation, percussion, and auscultation is appropriate. Diagnostic tests are becoming more complex, more expensive, and more inclined to separate the patient and physician. The stethoscope is still the more commonly used diagnostic medical instrument, but it is not always used to best advantage. It is familiar, harmless, portable, and inexpensive. Its appropriate use improves medical practice and reduces costs. Improvements in sound recording and analysis techniques have spurred a renewed interest in lung sounds and their meaning. This is likely to lead to better understanding of what we hear, and perhaps to the development of new noninvasive diagnostic and monitoring techniques.

Acute respiratory distress syndrome

If Pa:Fi < 300 mmHg (40 kPa), then the definitions recommended a classification as "acute lung injury" (ALI). Note that according to these criteria, arterial blood gas analysis and chest X-ray were required for formal diagnosis. Limitations of these definitions include lack of precise definition of acuity, nonspecific imaging criteria, lack of precise definition of hypoxemia with regards to PEEP (affects arterial oxygen partial pressure), arbitrary Pa thresholds without systematic data.

[Requirements in radiologic diagnosis from the internist-cardiology viewpoint].

The article discusses the demands to be made on the various radiological methods in thoracic diagnostics in respect of their informative value for therapeutic consequences, as seen from the viewpoint of internal-cardiological intensive-care medicine. The importance of x-ray thoracic film in one or two planes is emphasised, with special reference to routine imaging. In consideration of the demonstration of essential pathological findings, routine chest x-ray film would be mandatory only the 40th year of age onwards and lateral projection from the 50th year. At any rate, about 50% of routine thorax x-rays in intensive-care wards show changes, the percentage being higher if there is a clinical suspicion of changes. Mention must be made of a so-called time phase lag between the x-ray thoracic findings and changed pulmonary arterial pressure. In diagnosis of pulmonary artery embolism the nuclear medicine methods are compared with pulmonary arterial angiography, taking sensitivity and specificity into account. 90% of pulmonary embolism show only non-specific changes in the chest x-ray. Together with these and perfusion scintigraphy a sensitivity of 98% can be attained, albeit with lower specificity, since perfusion angiography and angiography agree in only about 87% of the cases. The demands to be made on radiological diagnostics must be determined from case to case by the diagnostic effectivity in relation to the technical setup and cost. The cost aspect of the individual methods is of major importance when installing equipment in hospitals.

Pulmonary heart disease

Signs and symptoms The symptoms/signs of pulmonary heart disease (cor pulmonale) can be non-specific and depend on the stage of the disorder, and can include blood backing up into the systemic venous system, including the hepatic vein. As pulmonary heart disease progresses, most individuals will develop symptoms like: Shortness of breath Wheezing Cyanosis Ascites Jaundice Enlargement of the liver Raised jugular venous pressure (JVP) Third heart sound Intercostal recession Presence of abnormal heart sounds Causes The causes of pulmonary heart disease (cor pulmonale) are the following: Acute respiratory distress syndrome (ARDS) COPD Primary pulmonary hypertension Blood clots in lungs Kyphoscoliosis Interstitial lung disease Cystic fibrosis Sarcoidosis Obstructive sleep apnea (untreated) Sickle cell anemia Bronchopulmonary dysplasia (in infants)

[Pulmonary sonography-a valuable supplement to basic diagnostics for timely outpatient clarification of cough and dyspnea].

Cough and dyspnea are among the most common symptoms in primary medical care and potentially threatening diseases must be excluded in a timely manner, especially acute heart failure and its causes, pneumonia, pleural effusion, pulmonary embolism and pneumothorax. Anamnesis, inspection, physical examination and technical basic diagnostics are usually sufficient for an initial risk stratification. A reliable suspected diagnosis can often be made in this way; however, it is not uncommon for the findings to be ambiguous. Chest X‑ray diagnostics and laboratory diagnostics are established as the standard approach for these situations; however, a major limitation of these diagnostic techniques is the lack of immediate availability in the general practitioner's office and laboratory results are not available until the next day or the day after. Furthermore, the sensitivity and specificity of these diagnostic procedures are limited but often overestimated, especially in the case of mild to moderately pronounced alterations and in early stages of a disease. Thoracic sonography can be used in these situations as a direct extension of the physical examination. Its diagnostic value is undisputed. The most important pathological findings, such as pleural effusion and subpleural consolidations can be immediately visualized with sufficient certainty using miniaturized handheld ultrasound devices. The concept of the ultrasound stethoscope, which has been under discussion for more than 15 years, can also be implemented as point-of-care ultrasound (POCUS). The POCUS will become established as routine diagnostics in the future, for example in emergency outpatient diagnostics. It is time for pulmonary ultrasound to be added to the repertoire of primary care diagnostics.

Emergency department

Asthma and COPD Acute exacerbations of chronic respiratory diseases, mainly asthma and chronic obstructive pulmonary disease (COPD), are assessed as emergencies and treated with oxygen therapy, bronchodilators, steroids or theophylline, have an urgent chest X-ray and arterial blood gases and are referred for intensive care if necessary. Noninvasive ventilation in the ED has reduced the requirement for tracheal intubation in many cases of severe exacerbations of COPD. Special facilities, training, and equipment An ED requires different equipment and different approaches than most other hospital divisions. Patients frequently arrive with unstable conditions, and so must be treated quickly. They may be unconscious, and information such as their medical history, allergies, and blood type may be unavailable. ED staff are trained to work quickly and effectively even with minimal information.