Perform urgent coronary angiography.

A 72-year-old woman presents to the hospital with oppressive chest pain of 2 hours' duration. Blood pressure is 68/32 mm Hg, heart rate is 124 beats/min, respiratory rate is 32 breaths/min, oxygen saturation is 91% with oxygen at 50%, bilateral crackles on pulmonary auscultation. An ECG shows a subepicardial lesion in the anterior face, with a specular image in the inferior face. Chest X-ray shows bilateral alveolar pattern. What is your therapeutic decision?

Perform fibrinolysis with tenecteplase (TNK).

Seventy-six-year-old man with progressive dyspnoea.

A 76-year-old man with 50 years of smoking history was diagnosed in 2012 with diffuse interstitial lung disease, with radiological data of usual interstitial pneumonia. He came to the emergency room presenting with progression of dyspnoea for 1 week, concomitant with loss of 5 kg of weight, anorexia and poor general condition. He had tachypnoea at rest (30 breaths/min), peripheral cyanosis, speech interfered by cough and breathlessness, baseline oxygen saturation 90%, heart rate 40 beats/min and blood pressure 130/70 mm Hg. Chest X-ray was performed and there was basal atelectasia of the right lung. ECG and urgent echocardiogram (transthoracic echocardiogram, TTE) were also performed (figure 1). Which of the following best explains the patient's situation?heartjnl;105/1/74/F1F1F1Figure 1(A) ECG. (B) Long-axis parasternal view from the transthoracic echocardiogram (TTE). (C) Four-chamber view from the TTE.Acute pulmonary embolismNon-ST elevation myocardial infarctionCardiac lymphomaCardiac myxomaMobitz type II AV block.

[Comments on the 2010 guidelines on cardiopulmonary resuscitation of the European Resuscitation Council].

Administer chest compressions (minimum 100/min, minimum 5 cm depth) at a ratio of 30:2 with ventilation (tidal volume 500-600 ml, inspiration time 1 s, F(I)O₂ if possible 1.0). Avoid any interruptions in chest compressions. After every single defibrillation attempt (initially biphasic 120-200 J, monophasic 360 J, subsequently with the respective highest energy), chest compressions are initiated again immediately for 2 min independent of the ECG rhythm. Tracheal intubation is the optimal method for securing the airway during resuscitation but should be performed only by experienced airway management providers. Laryngoscopy is performed during ongoing chest compressions; interruption of chest compressions for a maximum of 10 s to pass the tube through the vocal cords. Supraglottic airway devices are alternatives to tracheal intubation. Drug administration routes for adults and children: first choice i.v., second choice intraosseous (i.o.). Vasopressors: 1 mg epinephrine every 3-5 min i.v. After the third unsuccessful defibrillation amiodarone (300 mg i.v.), repetition (150 mg) possible. Sodium bicarbonate (50 ml 8.4%) only for excessive hyperkaliemia, metabolic acidosis, or intoxication with tricyclic antidepressants. Consider aminophylline (5 mg/kgBW). Thrombolysis during spontaneous circulation only for myocardial infarction or massive pulmonary embolism; during on-going cardiopulmonary resuscitation (CPR) only when indications of massive pulmonary embolism. Active compression-decompression (ACD-CPR) and inspiratory threshold valve (ITV-CPR) are not superior to good standard CPR. Most effective improvement of outcome by prevention of full cardiorespiratory arrest. Basic life support: initially five rescue breaths, followed by chest compressions (100-120/min depth about one third of chest diameter), compression-ventilation ratio 15:2. Foreign body airway obstruction with insufficient cough: alternate back blows and chest compressions (infants), or abdominal compressions (children >1 year). Treatment of potentially reversible causes: ("4 Hs and 4 Ts") hypoxia and hypovolaemia, hypokalaemia and hyperkalaemia, hypothermia, and tension pneumothorax, tamponade, toxic/therapeutic disturbances, thrombosis (coronary/pulmonary). Advanced life support: adrenaline (epinephrine) 10 µg/kgBW i.v. or i.o. every 3-5 min. Defibrillation (4 J/kgBW; monophasic or biphasic) followed by 2 min CPR, then ECG and pulse check. NEWBORNS: Initially inflate the lungs with bag-valve mask ventilation (p(AW) 20-40 cmH₂O). If heart rate remains <60/min, start chest compressions (120 chest compressions/min) and ventilation with a ratio 3:1. Maintain normothermia in preterm babies by covering them with foodgrade plastic wrap or similar. POSTRESUSCITATION PHASE: Early protocol-based intensive care stabilization; initiate mild hypothermia early regardless of initial cardiac rhythm [32-34°C for 12-24 h (adults) or 24 h (children); slow rewarming (<0.5°C/h)]. Consider percutaneous coronary intervention (PCI) in patients with presumed cardiac ischemia. Prediction of CPR outcome is not possible at the scene, determine neurological outcome <72 h after cardiac arrest with somatosensory evoked potentials, biochemical tests and neurological examination. ACUTE CORONARY SYNDROME: Even if only a weak suspicion of an acute coronary syndrome is present, record a prehospital 12-lead ECG. In parallel to pain therapy, administer aspirin (160-325 mg p.o. or i.v.) and clopidogrel (75-600 mg depending on strategy); in ST-elevation myocardial infarction (STEMI) and planned PCI also prasugrel (60 mg p.o.). Antithrombins, such as heparin (60 IU/kgBW, max. 4000 IU), enoxaparin, bivalirudin or fondaparinux depending on the diagnosis (STEMI or non-STEMI-ACS) and the planned therapeutic strategy. In STEMI define reperfusion strategy depending on duration of symptoms until PCI, age and location of infarction. TRAUMA: In severe hemorrhagic shock, definitive control of bleeding is the most important goal. For successful CPR of trauma patients a minimal intravascular volume status and management of hypoxia are essential. Aggressive fluid resuscitation, hyperventilation and excessive ventilation pressure may impair outcome in patients with severe hemorrhagic shock. Any CPR training is better than nothing; simplification of contents and processes is the main aim.

[Acute thoracic aortic dissection with occlusion of the left coronary artery].

Aortic dissection is the most common fatal condition that involves the aorta. Occasionally, symptoms mimic acute myocardial infarction leading to thrombolytic treatment. Accurate diagnosis in patients with chest pain is therefore essential. We describe a case of acute aortic dissection which resulted in myocardial infarction due to obstruction of the left coronary ostium. A 65-year-old female patient with no previous cardiac history was admitted to a local hospital because of severe chest pain of acute onset. Physical examination was normal except for a low blood pressure (90/50 mm Hg), heart rate 45 beats/min and parasthesia in both hands. The ECG showed sinus bradycardia with negative T-wave in VI and with 1 mm ST-segment elevation in V3. A chest X-ray was normal. Five hours later, the patient experienced once more severe chest pain followed by non-sustained polymorphic ventricular tachycardia (Figure 1). Another ECG showed bifascicular bundle branch block (right bundle branch block and left anterior fascicular block). The ECG was interpreted as showing acute myocardial infarction and treatment with intravenous streptokinase started. Since the patient remained severely hypotensive despite infusion of dobutamine, she was intubated, ventilated and transferred to our hospital. Cardiac catheterization showed acute dissection of the ascending aorta with an aortic intimal flap and an occlusion of the left coronary artery (Figures 2a and b). During catheterization, she suffered a cardiac arrest from which she could not be resuscitated. A postmortem examination confirmed the acute aortic dissection which reached to the ostium of the left coronary artery (Figures 3a and b, 4a and b) and an anterior myocardial infarction probably due to intermitted diastolic obstruction of the ostium of the left coronary artery by an aortic intimal flap.

Diagnostic computed tomography in acute interscapular pain.

Clinical introductionA man in his 60s with no medical history presented with sudden-onset, severe interscapular pain. He was in circulatory shock with a blood pressure of 65/30 mm Hg, heart rate of 115 beats per minute, respiratory rate of 32 breaths per minute and a room air oxygen saturation of 89%. Examination demonstrated weak peripheral pulses, an elevated jugular venous pressure, faint dual heart sounds, no cardiac murmurs and bilateral lung crepitations. An ECG was recorded which showed a broad QRS (figure 1A). There were no previous ECGs to compare this with. In view of his presentation with acute-onset interscapular pain, CT of the aorta was organised by the emergency department clinicians (figure 1B-D). After the CT result was obtained, the on-call cardiologist was contacted and a bedside echocardiogram performed. This demonstrated severe left ventricular systolic dysfunction with akinesia of the apex and lateral walls. The patient was then transferred to the catheter laboratory for an emergency invasive coronary angiogram.heartjnl;106/2/126/F1F1F1Figure 1ECG and CT images at presentation (A) 12 lead ECG. (B) Contrast enhanced CT aorta - coronal view. (C) Contrast enhanced CT aorta - axial view. (D) CT aorta showing 4 chamber view of the heart. WHAT IS THE MOST LIKELY DIAGNOSIS?: Pulmonary embolism.Aortic dissection.Acute myocardial infarction.Cardiac tamponade.

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.

InternalMed_Harrison

History of myocardial infarction Current angina considered to be ischemic Requirement for sublingual nitroglycerin Positive exercise test Pathological Q-waves on ECG History of PCI and/or CABG with current angina considered to be ischemic Left ventricular failure by physical examination History of paroxysmal nocturnal dyspnea History of pulmonary edema S3 gallop on cardiac auscultation Bilateral rales on pulmonary auscultation Pulmonary edema on chest x-ray History of transient ischemic attack History of cerebrovascular accident Treatment with insulin Abbreviations: CABG, coronary artery bypass grafting; ECG, electrocardiogram; PCI, percutaneous coronary interventions. Source: Adapted from TH Lee et al: Circulation 100:1043, 1999.

Spontaneous Hemoptysis in a Patient With COVID-19.

A 65-year-old man presented with shortness of breath, gradually worsening for the previous 2 weeks, associated with dry cough, sore throat, and diarrhea. He denied fever, chills, chest pain, abdominal pain, nausea, or vomiting. He did not have any sick contacts or travel history outside of Michigan. His medical history included hypertension, diabetes mellitus, chronic kidney disease, morbid obesity, paroxysmal atrial fibrillation, and tobacco use. He was taking amiodarone, carvedilol, furosemide, pregabalin, and insulin. The patient appeared to be in mild respiratory distress. He was afebrile and had saturation at 93% on 3 L of oxygen, heart rate of 105 beats/min, BP of 145/99 mm Hg, and respiratory rate of 18 breaths/min. On auscultation, there were crackles on bilateral lung bases and chronic bilateral leg swelling with hyperpigmented changes. His WBC count was 6.0 K/cumm (3.5 to 10.6 K/cumm) with absolute lymphocyte count 0.7 K/cumm (1.0 to 3.8 K/cumm); serum creatinine was 2.81 mg/dL (0.7 to 1.3 mg/dL). He had elevated inflammatory markers (serum ferritin, C-reactive protein, lactate dehydrogenase, D-dimer, and creatinine phosphokinase). Chest radiography showed bilateral pulmonary opacities that were suggestive of multifocal pneumonia (Fig 1). Nasopharyngeal swab for SARS-CoV-2 was positive. Therapy was started with ceftriaxone, doxycycline, hydroxychloroquine, and methylprednisolone 1 mg/kg IV for 3 days. By day 3 of hospitalization, he required endotracheal intubation, vasopressor support, and continuous renal replacement. Blood cultures were negative; respiratory cultures revealed only normal oral flora, so antibiotic therapy was discontinued. On day 10, WBC count increased to 28 K/cumm, and chest radiography showed persistent bilateral opacities with left lower lobe consolidation. Repeat respiratory cultures grew Pseudomonas aeruginosa (Table 1). Antibiotic therapy with IV meropenem was started. His condition steadily improved; eventually by day 20, he was off vasopressors and was extubated. However, on day 23, he experienced significant hemoptysis that required reintubation and vasopressor support.

[The role of 2D-doppler electrocardiography in the early diagnosis of massive acute pulmonary embolism and therapeutic monitoring].

Early diagnosis is important for the prognosis of patients affected with pulmonary embolisms. The mortality rate ranges from 30% in untreated cases to 10% in cases getting early treatment. In this context, it is essential to obtain a correct diagnosis in order to start the best treatment for each patient. The aim of our study is to evaluated the contribution of mono- bidimensional echocardiography and color-doppler for the early diagnosis of acute massive pulmonary embolism. We examined 23 patients (14 women with a mean age of 67 +/- 13 years; 9 men with a mean age of 58 +/- 16 years) who were referred to us for observation over a 30-month period. These patients had been admitted to the intensive care unit for suspected acute massive pulmonary embolism and the diagnosis was subsequently confirmed by a pulmonary scintigraphy. None of the 23 patients showed a positive case history of previous heart disease and/or pulmonary disease. The patients were checked using 2D-doppler echocardiography, 120 +/- 45 minutes from the onset of the symptoms. They were then divided into two groups (A and B) based on the presence or absence of thromboembolus in the right cavity of the heart. Seven patients (30%) revealed thromboemboli and were treated effectively with rt-PA (100 mg/2 hours). An increase in the size of the right ventricle with an affected rate RV/LV > 0.6 and the abnormal kinetics of the ventricular septum proved to be the most sensitive parameters for right ventricular overload, as signs of acute massive pulmonary ambolisms were observed in all 23 patients. Tricuspid regurgitation speed (from 2.9 to 3.6 m/sec) and peak systolic pulmonary pressure (67 mmHg) were recorded in all patients. Our observations suggest that the hemodynamic effects of an acute massive pulmonary embolism can be enumerated and monitored by analyzing ventricle size and septum kinetics. To summarize, echocardiography proved to be a simple and realistic test. It enabled correct diagnosis and made it possible not only to start thrombolytic therapy without requiring other exams, but also to monitor and evaluate the effects of this therapy.

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.

[Hemodynamic course during fibrinolysis in severe pulmonary embolism].

Seventy seven cases of severe pulmonary embolism (Miller index greater than 13 points) including 61 acute (under 5 days) and 16 subacute episodes, underwent continuous haemodynamic monitoring during treatment with either urokinase 2 000 U/kg/h for 24 hours with heparin (Group I: 18 patients), or urokinase 4 500 U/kg/h for 12 hours without heparin (Group II: 47 patients), or with streptokinase 2 00 000 U over 10 hours (Group III: 12 patients). Efficacy was defined as greater than 20% improvement of Miller index at control angiography after 48 hours (Group I: 10 patients, Group II: 31 patients, Group III: 8 patients). In the 49 patients (63%) with good results, the Miller index fell by about 50% with a significant increase in cardiac index (20%) from the 12th hour. There was a concomitant fall in pulmonary systolic arterial pressure (35%). In the 28 patients (37%) with partial improvement a 20% increase in cardiac index and an 18% fall in pulmonary systolic arterial pressure were observed only in the high dose urokinase group, despite incomplete pulmonary revascularisation demonstrating the vasodilator effect of this protocol. Fibrinolysis was repeated in the patients with incomplete results or a Miller index of over 13 points, leading to improvement in 78% of patients. Accelerated lysis of pulmonary embolism leads to rapid normalisation of haemodynamic parameters and improves the prognosis of massive pulmonary embolism by reducing the number of recurrences and the mortality rate (4%).

Twenty-three year-old with pleuritic chest pain.

A 23-year-old woman followed at another medical centre for congenital heart disease (CHD) presented to our emergency clinic with 3 weeks of bilateral pleuritic chest pain. She returned from holiday in Greece 6 weeks earlier where a tattoo and nasal piercing had been performed. There was no history of night sweats or fever.Her temperature was 37.5°C, heart rate 120 beats/min, oxygen saturations 94% on room air and blood pressure 110/74. Her chest was clear and there was systolic murmur on auscultation. The chest radiograph showed peripheral bilateral lower zone atelectasis. The ECG demonstrated sinus tachycardia. The haemoglobin was 11.2 g/dL, white cell count 10.18×10<sup9</sup/L, C-reactive protein 67 mg/L (normal <5 mg/L) and D dimer=430 ng/mL (normal <230 ng/mL).A pulmonary embolus was suspected and a CT pulmonary angiogram was performed (figure 1). Based on the CT findings, what is the most likely underlying congenital heart lesion in this patient?Bicuspid aortic valveCoarctation of the aortaFontan circulationParachute mitral valveVentricular septal defect heartjnl;105/6/464/F1F1F1Figure 1CT pulmonary angiogram (coronal views).

[Pulmonary thromboembolism angiographically confirmed: clinical and prognostic aspects].

The aim of this study was to evaluate the clinical profile and prognosis of patients with an angiographically proven thromboembolism. Data from 22 consecutive patients (13 males, 9 females; mean age 57.3 +/- 16.8 years) with pulmonary embolism confirmed by pulmonary angiography were reviewed. All our patients were previously submitted to non-invasive diagnostic procedures (blood examinations, EKG, chest x-ray, echocardiography). A V/Q scan was also performed in 5 patients. Fourteen patients were traditionally treated with heparin alone and the rest received thrombolytic therapy and heparin. Two patients had a thromboembolectomy. At discharge, all our patients were submitted to an oral anticoagulant therapy. The mean duration of the follow-up period was 26 +/- 12 months. The majority of the patients were in the 6th decade of life and it was possible to identify a hypercoagulable state in 82%. The most common symptom at the time of presentation was sudden chest pain (64%). The most specific sign in non-invasive procedures were right side cardiac dilatation seen echocardiographically (73%) and the mismatch in the V/Q scan (80%). The most common haemodynamic parameter (91%) observed in the right heart catheterization of these patients was the finding of a gradient between diastolic pulmonary artery and pulmonary capillary wedge pressures. Uneventful angiography was performed in all patients who showed massive pulmonary embolism (86%). Three patients (13.6%) died during the acute phase. At the end of the follow-up period, 10 patients were asymptomatic and 5 had heart failure. Four died, which corresponds to an overall mortality of 31.8% in 2.2 years of follow-up. None of the clinical or haemodynamic parameters analyzed (age, gender, arterial blood gases at presentation, hypercoagulable states, thrombolysis, pulmonary hypertension and extension of the embolism) were related to mortality. Angiographically confirmed pulmonary thromboembolism is still a poor outcome situation, even when a lot of diagnostic and therapeutic procedures are available.

Peculiar mechanical complication of myocardial infarction.

A 58-year-old man presented to the chest pain unit with crescendo angina over 24 hours and worsening dyspnoea of 10 hours duration. He was a known diabetic and hypertensive on regular treatment for 10 years and a habitual smoker with over 15 pack-years smoking duration. Examination revealed a profusely diaphoretic and dyspnoeic (respiratory rate of 45/min) individual with a blood pressure of 100/60 mm Hg and heart rate of 124 beats/min. He was hypoxic and his oxygen saturation in the ambient air was 64%. His jugular venous pressure was elevated with a prominent V wave. Cardiovascular examination revealed a harsh grade IV/VI systolic murmur over the lower left parasternal border. There were bilateral extensive crepitations heard over the lung fields. ECG on admission revealed presence of Q wave and ST elevation in leads II and III, aVF with ST depression in I and aVL. X-ray chest showed normal cardiac shadow and features of grade III pulmonary venous hypertension. Transthoracic echocardiography is shown in figure 1.Figure 1Transthoracic echocardiogram short axis view at mid cavity level, 2D (A) and colour Doppler (B) image. <bWhat is the most likely diagnosis</b?A. Left ventricular (LV) true aneurysmB. LV pseudoaneurysmC. LV pseudo-pseudoaneurysmD. Ventricular septal rupture (VSR)E. LV free wall rupture.

[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.

PCR use in miliary tuberculosis presenting with acute respiratory distress syndrome.

A 30-year-old pregnant woman admitted to the hospital for rapidly progressive dyspnoea, non-productive cough and altered general status evolving over 1-month period. Her vital signs showed a low blood pressure 90/60 mm Hg, pulse rate 100 beats/min, respiratory rate 32 breaths/min and oxygen saturation on room air of 88%. Laboratory findings showed haemoglobin 9.7 g/dl, white blood cells 15 000/mm(3) (neutrophils 82%), C reactive protein 74 mg/l, alkaline phosphatase 320 U/l, alanine aminotransferase 62 IU/l, aspartate aminotransferase 120 IU/l, γ glutamyl transpeptidase 125 U/l; brain natriuretic peptide 25.4 pg/ml, procalcitonine >2, lactate dehydrogenase 1618 U/l. Chest radiographics showed diffuse bilateral micronodular pulmonary infiltrates and CT of the chest confirmed 1-3 mm diffuse bilateral micronodular infiltrates with ground glass opacities. Complete investigation including bronchoalveolar lavage (BAL) for any viral, bacteriologic, acid-fast bacilli and full serum antibodies panel were all negative. DNA amplification for mycobacterium using PCR on the BAL rapidly rectified the diagnosis of tuberculosis.

[Massive pulmonary embolism--echocardiographic diagnosis and thrombolytic therapy].

Thrombolysis is widely accepted as the treatment of choice for acute massive life-threatening pulmonary embolism. Several trials have shown that thrombolytic treatment has reduced morbidity and mortality in this condition, compared to heparin therapy. Rapid diagnosis and treatment start is mandatory for improving the prognosis. Clinical presentation, ECG, arterial blood gas analysis and D-dimer are non-specific tests. Additional tests like ventilation/perfusion lung scan, spiral-computed tomography or pulmonary angiography are needed. In an emergency situation a non-invasive and bedside technique is preferred, and several studies have demonstrated the accuracy of echocardiography in pulmonary embolism. Acute right ventricular overload is indicated by different echocardiographic findings. Three cases with the echocardiographic method as the initial technique for the diagnosis of massive pulmonary embolism are described as well as the treatment consequence and practical administration of thrombolysis. Our patients had presenting features suggestive of massive pulmonary embolism, a clinical situation where an echocardiographic evaluation is appropriate. All presented with typical echocardiographic features. Thrombolytic treatment was initiated immediately after echocardiographic diagnosis. Different thrombolytic regimens were used. Echocardiography may be used as the initial imaging technique for the diagnosis of massive pulmonary embolism. The advantages are obvious, and thrombolytic treatment can be initiated without delay.

Primary neuroendocrine tumour of the right ventricle presenting with heart failure and cyanosis.

A 68-year-old woman presented to the emergency department owing to exertional dyspnoea and bilateral leg oedema for 3 weeks. Her vital signs included the following: heart rate of 95 bpm, respiratory rate of 24 breaths/min, oxygen saturation of 73% on room air and a blood pressure of 184/108 mm Hg. Physical examination revealed tachypnoea with clear lungs to auscultation, elevated jugular veins, cyanosis and bilateral pitting oedema. A chest X-ray demonstrated cardiomegaly without obvious pulmonary oedema. A CT of the chest was negative for pulmonary embolus; however, the scan did reveal a large right ventricular (RV) mass. An echocardiogram with bubble study confirmed a patent foramen ovale with significant right-to-left shunting and a large RV mass that significantly obstructed the pulmonary outflow tract. A cardiac biopsy revealed a low-grade neuroendocrine tumour. The patient underwent successful debridement and adjuvant chemotherapy. She improved greatly and was asymptomatic at a 9-month follow-up visit.

[Disseminated coronary occlusions and massive pulmonary embolism in a 40-year-old woman].

A 40-year-old woman was admitted to the emergency room because of severe angina pectoris and dyspnoe at rest. She developed ventricular fibrillation a few minutes later from which she had to be resuscitated . After intubation and controlled ventilation immediate angiocardiography was performed while she was still in cardiogenic shock. Coronary angiography ten days before had been unremarkable. The second coronary angiogram revealed severe thrombotic lesion at the origin of the left anterior descending branch (LAD) and total occlusions of the peripheral LAD and of the first marginal branch. After intracoronary application of 10 mg abciximab and coronary stent implantation in the origin of the LAD the patient had good clinical improvement. Massive pulmonary embolism two days later, despite of effective heparinization and inhibition of platelet aggregation (as measured by partial thromboplastin time), was treated successfully by regional injection of 100 mg tissue plasminogen activator (t-PA). Tests for possible hypercoagulability showed no detectable changes in the clotting and fibrinolytic system with a normal platelet count. In a standardized aggregation test of platelets hyperaggregation in response to ADP and epinephrine, also at low test doses, revealed the presence of a sticky platelet syndrome. This case history suggests that enhanced platelet aggregation associated with sticky platelet syndrome may provoke myocardial infarction even in angiographically normal coronary arteries.

[Successful perioperative use of noninvasive positive pressure ventilation in a pregnant woman with acute pulmonary edema].

A 32-year-old woman (148 cm, 59 kg, gravida 2, para 2) with quadruplet pregnancy was admitted to our hospital for the threatened preterm labor at 23 weeks and 2 days of gestation. She was treated with ritodrine, magnesium sulfate and nifedipine to maintain tocolysis. Betamethasone was administered to accelerate fetal lung maturity. After ritodrine dose was increased at 23 weeks and 5 days of gestation, she developed dyspnea with desaturation. Acute pulmonary edema was revealed on chest X-ray. The decision was made to proceed with emergency cesarean delivery. On arrival at the operating room, the blood pressure was 123/53 mmHg, heart rate 111 beats x min(-1), and oxygen saturation (SpO2) 84% with supplemental oxygen 15 l x min(-1) via a reserved face mask. Noninvasive positive pressure ventilation (NPPV) was initiated with S/T mode (FIO2 1.0, inspiratory positive airway pressure 10 cmH2O, expiratory positive airway pressure 6 cmH2O). The dyspnea was improved with her SpO2 100%. Spinal anesthesia was performed at L 34 using 2.5 ml of 0.5% bupivacaine and 100 microg morphine. Throughout the operation (operation time 44 minutes), she did not develop dyspnea under NPPV. NPPV was discontinued after the operation. Her SpO2 declined, and pulmonary edema on chest X-ray was exacerbated. She was transferred to the intensive care unit and NPPV was continued for 22 hours after the operation. She was discharged from the intensive care unit on the next day and was discharged from the hospital on the 6th postoperative day.

Blunt rupture of the thoracic duct after severe thoracic trauma.

A 53-year-old man was admitted to our trauma center after sustaining thoracoabdominal injuries, secondary to a rear-end motor vehicle collision. As he stepped out of his vehicle, he was struck by a tractor trailer at 55 mph. The following were the initial vital signs on his arrival: heart rate 140 beats/min, blood pressure 142/80 mm Hg, respiratory rate 28 breaths/min, temperature 36.8°C, and oxygen saturation 93%. The Glasgow Coma Scale score was 15 and the Injury Severity Score was 59. He was evaluated and resuscitated per the advanced trauma life support protocols. The focused assessment with sonography for trauma examination was negative. Initial findings included bilateral chest wall and thoracic spine tenderness, subcutaneous emphysema in the chest and neck, and an unstable pelvis. He required bilateral chest tubes and a pelvic binder. CT imaging revealed a left temporal epidural hematoma, multiple facial fractures, a sternal fracture, a left scapula fracture, acromioclavicular fractures, bilateral hemopneumothoraces, pulmonary contusions, extensive pneumomediastinum compressing the right atrium, multiple rib fractures (2-10 on the left with a flail segment and 2-8 on the right) (figure 1), an unstable open-book pelvic fracture which included bilateral superior and inferior pubic rami fractures, sacral and left iliac wing fractures, and symphysis pubis diastasis.Figure 1Three-dimensional CT scan reconstruction demonstrating left-sided flail chest.The patient developed hypotension and severe respiratory distress, and was intubated. ECG revealed no dysrhythmias. Echocardiogram revealed significant left ventricular wall dysfunction consistent with myocardial contusion and right atrial compression. His troponins were also significantly elevated. He required significant resuscitation with crystalloids, blood products and vasopressors. He underwent bronchoscopy, esophagram and upper endoscopy to exclude tracheoesophageal injury, and these were negative. On hospital day 2, the patient was hemodynamically stable, and pressors were discontinued. His pelvic fractures were repaired using external fixation and sacral screws. Given his extensive left flail chest, he underwent reconstruction of his left chest wall on hospital day 5. Open reduction and internal fixation of his left ribs, 3 to 6 anteriorly and 4 to 7 posteriorly, with titanium plates was performed (figure 2). He had an epidural catheter inserted for analgesia. On postoperative day 2 after chest wall reconstruction, the patient was extubated and resumed enteral feeds. Overnight, the output from the left-sided chest tube changed from serosanguinous to milky. A sample was sent for triglycerides and lymphocyte counts confirming the diagnosis of chylothorax. His chest tube output increased to approximately 2000 mL/day. A lymphangiogram was performed with Lipiodol to diagnose the location of the chylous leak. It revealed contrast extravasation at the level of T3 to T4. An MRI was also performed to better define the anatomic course of the thoracic duct.Figure 2Postoperative chest X-ray demonstrating left chest wall reconstruction. Conservative management: placing the patient nulla per os (NPO), and starting total parenteral nutrition (TPN), octreotide and midodrine.Thoracic duct embolization by interventional radiology.CT-guided thoracic duct disruption.Thoracotomy with thoracic duct ligation.

[The diagnostic and therapeutic procedures in pulmonary embolism: a survey in the Veneto Region].

Pulmonary embolism is one of the most frequent cardiopulmonary diseases, but it is often under- or misdiagnosed. In order to address this issue and to identify flow charts that are commonly used in pulmonary embolism diagnosis and treatment, 191 clinical wards of internal medicine, cardiology, geriatrics, pneumology and intensive care units, located in the Veneto Region, were surveyed. An anonymous questionnaire was mailed to each ward in order to collect clinical diagnostic information on all pulmonary embolisms which occurred during 1993. Among the returned questionnaires, 114 (59.6%) had usable information for the analysis. The vast majority of participating centers reported in 1993 less than 10 pulmonary embolism events. No significant differences were observed between internal medicine, geriatrics, pneumology wards and intensive care units. The reported events, however, were slightly higher in the divisions of cardiology with an annual average of 12 events per center. First level diagnostic procedures, such as ECG, chest X-ray and arterial blood gas analysis were chosen and performed in all patients. Interestingly, Doppler echocardiography, which is often not included in official guidelines for pulmonary embolism diagnosis, was performed in 56% of the participating centers. On the contrary, ventilation-perfusion lung scanning, which is considered highly predictive in many diagnostic algorithms, was underutilized (35% perfusion scan, 20% ventilation scan). This underuse was probably due to technical and organizational difficulties. Pulmonary angiography, the most accurate procedure for the diagnosis of pulmonary embolism, was performed in 28% of the patients. During the acute phase, intravenous heparin was commonly used; 91% of patients received the infusion continuously, 4% intermittently. Thrombolysis was performed in 25% of the patients. The preferred drugs were recombinant tissue-plasminogen activator (67%), followed by urokinase (20%) and streptokinase (13%). To start thrombolytic therapy, 20% of the interviewed clinicians considered sufficient the evidence of clinical manifestations of pulmonary embolism confirmed by echocardiographic data. At discharge, prescription of oral anticoagulant drugs was common (78%) for at least 6 months (47%). Standardized procedures for the diagnosis and treatment of pulmonary embolism were already implemented in 13% of the participating centers. These data suggest a common effort to define unanimous conventional protocols in the management of pulmonary embolism. It should be underlined, however, that a particular attention to the clinical manifestations and a productive collaboration among clinicians with different expertise are required to improve the diagnosis and treatment of pulmonary embolism.

Phoneutria

A 3-year-old girl, bitten on the third finger of her right hand, presented immediate local pain, periods of alternating prostration, cold sweating, chest and abdomen pains and 3 episodes of vomiting, was admitted to UNICAMP 3 hours after the accident, with the same symptoms, except for vomiting, 5 vials of AV (Antivenom) and local anesthetic infiltration were administered, there was an improvement in symptoms, with decrease in sweating, but still agitated, 2-3 hours after AV, there was a picture of significant diarrhea (stools semi-liquids) evolving to 2nd degree dehydration, parenteral hydration was started, 3h30 min post AV, heart rate was 160 beats, and respiratory rate was 72, 4 hours post AV, she had peripheral cyanosis, heart rate 150 beats and dyspnea , and loss of peripheral venous access, 4h15-4h30 min there was disseminated pulmonary stortoration, and worsening of agitation, dyspnea and bradycardia, being performed orotracheal intubation, manual ventilation, adrenaline and

Man in his 50s with chest pain and dyspnoea.

A man in his 50s with sudden-onset chest pain and dyspnoea was transferred to the emergency room. He had a history of aortic valve replacement due to aortic regurgitation with a mechanical valve 6 years previously. Heart rate was 90 bpm, and blood pressure was too low to measure. In the emergency room, he presented with severe dyspnoea and a chest X-ray showed severe lung congestion (figure 1A). ECG showed complete left bundle branch block. His respiratory status rapidly worsened, and he went into cardiopulmonary arrest. After cardiopulmonary resuscitation, transthoracic echocardiography was performed (figure 1B, online supplementary video 1).DC1SP110.1136/heartjnl-2017-312477.supp1Supplementary file 1 heartjnl;104/10/868/F1F1F1Figure 1(A) Chest X-ray. (B) Colour Doppler image from apical five-chamber view. What is the most likely cause of the patient's cardiopulmonary arrest?Myocardial infarction in left main trunkAortic dissectionProsthetic valve thrombosisProsthetic valve embolisationPulmonary embolism.

[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.

High-flow nasal cannula oxygen therapy in the management of acute respiratory distress syndrome secondary to opioid overdose.

In this article, we discuss the successful treatment of acute respiratory distress syndrome (ARDS), a rare complication of opioid overdose, through high-flow nasal cannula oxygen therapy (HFNCOT). A 32-year-old male patient was referred to the emergency department with an ambulance due to a state of confusion following intravenous opioid intake. On arrival, the patient had an arterial blood pressure of 100/60 mmHg, pulse of 112 beats/min, respiratory rate of 8 breaths/min, and oxygen saturation (SpO<sub2</sub) of 75%. On neurologic examination, he had miotic and isochoric pupils, and Glasgow Coma Score was 12 (E: 3 M: 5 V: 4). Cardiac examination showed that the heart was rhythmic and tachycardic. Chest examination revealed bibasilar crackles and wheezing. Naloxone was administered to the patient, and oxygen treatment was applied through a mask. Then, HFNCOT was commenced to the patient in whom the PaO<sub2</sub/FiO<sub2</sub ratio in the blood gas was calculated as 141 following antidote treatment and whose chest radiograph showed bilateral infiltrations. The patient was discharged from the emergency critical care unit on the 3<suprd</sup day of his hospitalization because infiltrations in his chest radiograph regressed. HFNCOT can recover the patient's hypoxemia and help reduce the necessity of mechanical ventilation in patients with mild or moderate ARDS.

History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease.

The history and physical examination were assessed in 215 patients with acute pulmonary embolism uncomplicated by preexisting cardiac or pulmonary disease. The patients had been included in the Urokinase Pulmonary Embolism Trial or the Urokinase-Streptokinase Embolism Trial. Presenting syndromes were (1) circulatory collapse with shock (10 percent) or syncope (9 percent); (2) pulmonary infarction with hemoptysis (25 percent) or pleuritic pain and no hemoptysis (41 percent); (3) uncomplicated embolism characterized by dyspnea (12 percent) or nonpleuritic pain usually with tachypnea (3 percent) or deep venous thrombosis with tachypnea (0.5 percent). The most frequent symptoms were dyspnea (84 percent), pleuritic pain (74 percent), apprehension (63 percent) and cough (50 percent). Hemoptysis occurred in only 28 percent. Dyspnea, hemoptysis or pleuritic pain occurred separately or in combination in 94 percent. All three occurred in only 22 percent. The most frequent signs were tachypnea (respiration ate 20/min or more) (85 percent), tachycardia (heart rate 100 beats/min or more) (58 percent), accentuated pulmonary component of the second heart sound (57 percent) and rales (56 percent). Signs of deep venous thrombosis were present in only 41 percent and a pleural friction rub was present in only 18 percent. Either dyspnea or tachypnea occurred in 96 percent. Dyspnea, tachypnea or deep venous thrombosis occurred in 99 percent. As a group, the identified clinical manifestations, although nonspecific, are strongly suggestive of acute pulmonary embolism. Conversely, acute pulmonary embolism was rarely identified in the absence of dyspnea, tachypnea or deep venous thrombosis.

TIMI

TIMI Risk Score for STEMI Age 65-74 years? Yes (+2) – or – Age ≥75 years? Yes (+3) Diabetes, Hypertension or Angina? Yes (+1) Systolic BP < 100 mmHg? Yes (+3) Heart rate > 100? Yes (+2) Killip Class II-IV (JVD or any pulmonary exam findings of CHF)? Yes (+2) Weight < 67kg (147.7 lbs)? Yes (+1) Anterior ST Elevation or LBBB? Yes (+1) Time to treatment > 4 hours? Yes (+1) What Does This Score Mean? TIMI Risk Score for HF in Diabetes Prior heart failure? Yes (+2) History of atrial fibrillation? Yes (+1) Coronary artery disease? Yes (+1) eGFR < 60 ml/min/1.73*m2? Yes (+1) Urine albumin-to-creatinine ratio >300 mg/g? Yes (+2) – or – Urine albumin-to-creatinine ratio 30-300 mg/g? Yes (+1) What Does This Score Mean?

Severe hypertension and pulmonary edema associated with systemic absorption of topical phenylephrine in a child during retinal surgery.

Topical phenylephrine solutions are widely used in eye procedures to promote pupil dilation without cycloplegia. We report a case of intraoperative severe hypertension and acute pulmonary edema occurring in a child during retinal surgery after possible systemic absorption of topical phenylephrine eyedrops. Our objective is to discuss the proper treatment and preventive strategies for such a complication. A 4-year-old, male patient, 18.4 kg in weight, physical status ASA I was admitted for right retinal detachment surgery. Anesthesia was induced with sevoflurane in oxygen, followed by glycopyrrolate (5.0 μg/kg), propofol 25 mg, fentanyl 50 μg and cisatracurium 0.15 mg/kg given intravenously. Anesthesia was maintained with sevoflurane 2-2.5% in a mixture of nitrous oxide and oxygen (60%:40%). After incision, two drops of 10% aqueous phenylephrine were administered topically by the surgeon to the right eye for further pupil dilation. Few minutes later, the noninvasive blood pressure rose to 220/120 mmHg and the heart rate increased to 140 beats/min. Oxygen saturation (SpO(2)) dropped from 99% (with an inspired oxygen concentration (FiO(2)) of 0.4) to 82%. Auscultation revealed crepitations throughout the chest and a blood-stained frothy fluid was aspirated from the trachea with possible development of acute pulmonary edema. Hydralazine (5 mg) and furosemide (10 mg) were administered intravenously. Seven minutes later, the blood pressure returned to normal and the SpO(2) increased to 92% on FiO(2) of 1.0, with decreased intratracheal secretions. After approximately 20 minutes, the SpO(2) had improved to 99%, with a FiO(2) of 1.0 and the blood pressure was 109/63 mmHg and heart rate was 121 beats/min. The FiO(2) gradually reduced back to 0.4 over 30 min with no further desaturation. The patient was discharged from the post anesthesia care unit 5 h after surgery with adequate spontaneous breathing, SpO(2) 99% on room air, normal blood pressure and pulmonary auscultation. Anesthesiologists and ophthalmologists should be aware of the possible cardiovascular side-effects of topical phenylephrine, and it should be used cautiously with appropriate intraoperative monitoring of hemodynamic variables. Moreover, preventive strategies to minimize systemic absorption of the drug should be taken.

[Normal coronary angiogram in patient with diagnosis of acute coronary syndrome with ST segment elevation. Was it possible to recognise acute pulmonary embolism earlier?].

A case of a 48 year old male scheduled for early invasive treatment of acute coronary syndrome with ST segment elevation is presented. Clinical suspicion of acute pulmonary embolism was undertaken because of normal coronary angiogram and was confirmed by pulmonary angiography. Differential diagnosis based on medical history, electrocardiogram and laboratory findings was discussed.

[Acute massive pulmonary embolism--report of a case].

A 72-year-old female, who had received medication for hypertension and angina pectoris was hospitalized with complaining of an abrupt dyspnea. Roentgenogram of the chest revealed no abnormal findings except cardiac enlargement. An electrocardiogram showed overloading of the right ventricle. Arterial blood gas analysis of room air showed 55.4 mmHg of PaO2, 25.5 mmHg of PaCO2 and 7.30 of PH, respectively. Acute and massive pulmonary embolism was diagnosed by an emergent pulmonary arteriography. Despite intensive treatment such as infusion of urokinase and heparin for four days, thrombus was still detected in the left main pulmonary artery by a transesophageal echocardiography. By the result of ineffective conservative therapy, embolectomy was performed under cardiopulmonary bypass. However mechanical respiratory support was required for a long time due to the right heart failure, she is doing well for a year after the operation.

Resuscitation of hemorrhagic shock with hypertonic saline/dextran or lactated Ringer's supplemented with AICA riboside.

Anesthetized and ventilated swine were bled 23 ml/kg (34% of calculated blood volume) to a mean arterial pressure < 50 mm Hg. After 60 min, a bolus of either 7.5% hypertonic saline/6% dextran 70 (HSD, 4 ml/kg x 5 min) or lactated Ringer's (LR, 32 ml/kg x 5 min) was infused i.v. LR (25-30 ml/kg) was administered to all animals for the next 60 min. Amino imidazole carboxamide riboside (AICAR), which increases endogenous adenosine in ischemic tissues, was added to the initial bolus and the subsequent LR (10 mg/kg bolus + 0.5 mg/kg x 60 min) in half the study population. At 2 hr post-shock, hematocrit, urine output, arterial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, portal venous O2 saturation, and pulmonary arterial O2 saturation were similar in all groups. With HSD vs. LR, cardiac outputs and stroke volumes were each significantly higher, while right atrial pressures and pulmonary vascular resistances were each significantly lower, which is consistent with augmented cardiac contractility with HSD. Furthermore, systemic oxygen consumptions were significantly higher, and intracranial pressures were each significantly lower with HSD. Nevertheless, no variables were far outside the normal range in either group. The addition of AICAR to LR and HSD eliminated the difference in intracranial pressure, systemic oxygen consumption, reduced heart rate by 30-40 beats/min during the first hour of resuscitation, and increased stroke volume by 20-30%.(ABSTRACT TRUNCATED AT 250 WORDS)

Emergency department management of pulmonary embolism.

There are several points that bear repetition. First, consider the diagnosis of PE in all patients presenting with chest pain, dyspnea, syncope, oxygen desaturation, or unexplained hypotension. Evaluate these patients in a rational manner. At any individual hospital, develop algorithms with consultants so that when one is faced with a patient with a PE, the flow of both diagnostics and therapeutics flows smoothly and rapidly. Consider the concept of risk stratification, and remember that not all patients with PE are created equal. In particular, be on the same page with all consultants regarding the use of right heart echocardiography, both for its potential diagnostic capabilities and for its ability to identify patients who could be at greater risk for bad outcomes.