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Query: UMLS:C0034065 (pulmonary embolism)
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Pulmonary vascular congestion or pulmonary embolism in humans produces shallow tachypnea, and indirect experimental evidence suggests that this characteristic breathing pattern may result from activation of vagal unmyelinated afferents from the lung. We have investigated, in decerebrate cats, reflex changes in breathing pattern and in the activation of the diaphragm, posterior cricoarytenoid, and thyroarytenoid muscles caused by activating C-fiber afferents in the vagus nerve. The right vagus nerve was sectioned distal to the origin of the recurrent laryngeal nerve, eliminating vagal afferent traffic although preserving motor innervation of the larynx on that side. The left cervical vagus was stimulated electrically, and efferent activation of the laryngeal muscles was avoided by cutting the left recurrent laryngeal nerve. Transmission to the brain of vagal afferent traffic resulting from this stimulation was controlled by graded cold block of the nerve cranial to the site of application of the stimulus. Activation of C-fibers, when A-fibers were blocked, significantly decreased respiratory period and amplitude of diaphragm inspiratory burst. In addition, this selective activation of vagal C-fibers augmented postinspiratory activity of the diaphragm and recruited phasic expiratory bursts in the thyroarytenoid. We conclude that, in unanesthetized decerebrate cats, afferent traffic of vagal C-fibers initiates a pontomedullary reflex that increases respiratory frequency, decreases tidal volume, and augments braking of expiratory airflow.
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PMID:Stimulation of vagal C-fibers alters timing and distribution of respiratory motor output in cats. 260 30

The vasculature of one lung of unanesthetized spontaneously breathing decerebrate cats was isolated and congested with blood. Such pulmonary vascular congestion (PVC) consistently resulted in a shallow tachypnea associated with expiratory activation of the diaphragm and thyroarytenoid muscles, signifying augmented expiratory braking. With progressive increases in pulmonary vascular pressure, tachypnea and expiratory braking increased progressively and ultimately obscured phasic activity in the diaphragm and thyroarytenoid. Thus the apnea caused by PVC constitutes not an arrest of neural respiratory activity but rather a continuous activation of thoracic inspiratory and laryngeal adductor muscles. When capsaicin, a neurotoxin that activates nonmyelinated afferents, was injected into the pulmonary artery of the isolated lung, it produced changes in timing and distribution of respiratory motor output that resembled those with PVC but were more abrupt in onset. Capsaicin, applied perineurally to the cervical vagi, preferentially blocked the conduction of nonmyelinated afferent fibers. This procedure, which produced little degradation in Hering-Breuer reflexes, eliminated tachypnea and expiratory braking caused by PVC or capsaicin injection. The results indicate that activation of pulmonary vagal afferent fibers of C or A-delta category in unanesthetized cats reflexly modifies the respiratory motor output in a way that resembles the human response to PVC or pulmonary embolism. This is a brain stem reflex.
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PMID:Rapid shallow breathing caused by pulmonary vascular congestion in cats. 260 31

The overall incidence of pulmonary embolism (PE) among neurosurgical in-patients, whose ages ranged from 23 to 80, was 0.7%. Our report here is based on five cases of patients with PE. Four of these five patients were over 50 years of age. They had been admitted because of such reasons as brain tumor, spinal cord injury, intracerebral hematoma, and venous sinus thrombosis. Deep vein thrombosis (DVT) was seen in four but none were diagnosed before they had developed PE. Decreased level of consciousness and prolonged bed rest appeared to be common risk factors for PE. Mean duration between admission and onset of PE was 31 days. Although non-specific, tachycardia, tachypnea and hypoxemia were the most common signs and symptoms. As a definitive diagnostic procedure, pulmonary angiography was performed in most of cases. One patient required surgical embolectomy and others were treated with anticoagulation or fibrinolytic agents. In order to prevent recurrent thromboembolic phenomena, ligation of the inferior vena cava was a useful mode of treatment when anticoagulation was not indicated. And this approach seemed to be valid in most neurosurgical patients. We conclude that PE and DVT were not uncommon complications among Japanese neurosurgical patients and they can be treated successfully in collaboration with a cardiovascular surgeon if the diagnosis can be made correctly.
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PMID:[Pulmonary embolism as a complication in neurosurgical patients]. 261 3

An accurate diagnosis of pulmonary embolism is essential to prevent excessive mortality and morbidity from lack of therapy or inappropriate anticoagulation. The clinical diagnosis is highly nonspecific because none of the symptoms or signs of pulmonary embolism is unique and all may be caused by other cardiorespiratory disorders. The diagnosis of pulmonary embolism is unlikely, however, if patients do not have dyspnea, tachypnea, evidence of deep vein thrombosis, or a recognized predisposition to thromboembolic disease. Objective testing is mandatory to either confirm or exclude a diagnosis of pulmonary embolism. The electrocardiogram, chest X-ray and the echocardiogram may assist by excluding other potential diagnoses. Routine laboratory studies and lung function testing including blood gas analysis will not be of much help in the differential diagnosis. The hemodynamic investigation with a floating catheter is of diagnostic value especially in those cases where it is not possible to obtain the definitive diagnosis immediately; this method as well as echocardiography can provide a rough estimate of the degree of pulmonary vascular obstruction and are thus able to guide therapy. Methods such as DSA, CT, MR, SPECT, or radiolabelled thrombus scanning are promising but require more extensive validation before routine use. Lung scanning, with its high sensitivity but low specificity is a very useful procedure but cannot be considered to have diagnostic significance independent of the clinical situation. Pulmonary angiography provides the greatest diagnostic certainty of any test available. Based on current knowledge, a diagnostic approach for the management of clinically suspected pulmonary embolism is proposed. Ventilation-perfusion lung scanning is the appropriate next step after ECG, chest X-ray and echocardiogram. The finding of a normal perfusion scan rules out clinically significant embolism and anticoagulation is withheld. Segmental or lobar perfusion defects with normal ventilation in an appropriate clinical setting is sufficiently indicative of pulmonary embolism to proceed with therapy in patients without contraindications. Ventilation-perfusion scans of low or indeterminate probability for pulmonary embolism neither confirm nor exclude the presence of embolism and pulmonary angiography would then be the definitive procedure. As an alternative approach instrumental examination of the leg veins (with venography, impedance plethysmography, or ultrasound) is proposed (Figure 1). If these tests confirm the presence of deep venous thrombosis, anticoagulation can be commenced without the need to perform pulmonary angiography.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The diagnosis of lung embolism]. 265 57

One or several syncopes were the reason for hospitalization in 31 of 155 in-patients with proven pulmonary embolism. In all of them there were at least two further pointers to acute pulmonary embolism: all had tachypnoea, 28 had dyspnoea, 25 had sinus tachycardia (more than 100 beats/min), 24 had congested neck veins and 16 had deep leg-vein thrombosis. In 21 patients the ECG had signs of right heart strain, in 15 of 20 in whom it was measured the arterial oxygen partial pressure was below 70 mm Hg. In 23 patients the chest X-ray was largely unremarkable despite dyspnoea. In 23 patients there had been a massive embolus and 16 patients had died. Although syncope is only rarely caused by pulmonary embolism, its ominous significance in this connection should stimulate a search for further diagnostic pointers to such an occurrence.
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PMID:[Syncope as a misinterpreted leading symptom of pulmonary embolism]. 394 10

Despite technological progress, the clinical diagnosis of acute pulmonary embolism (APE) is often problematic, There are no typical or specific clinical cardiopulmonary symptoms or signs that serve for the diagnosis, and only the absence of tachypnea seems to be an important exclusion criterion. Electrocardiogram, laboratory tests (including circulatory markers of thromboembolic disease) and blood gas analysis are also unspecific. Chest X-ray provides a high incidence of suggestive abnormalities and remains the most helpful routine procedure. While the negative perfusion lung scan is the best procedure for exclusion of APE, the positive scan suffers from too low specificity to be of real interest. In contrast, pulmonary angiography is the diagnostic method of choice. Besides detection of pulmonary emboli and of the extent of perfusion abnormalities, pulmonary angiography allows measurement of useful parameters of cardiac and pulmonary function, precise monitoring of evolution and administration of selective thrombolytic therapy. The diagnostic value of recent noninvasive diagnostic procedures in APE (echocardiography, Doppler echocardiography, computer tomography, plethysmography) is briefly discussed.
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PMID:[Clinical picture and diagnosis of pulmonary embolism]. 639 26

In a retrospective study over the years 1978-1982, 729 cases of acute pulmonary embolism were analyzed in relation to history, clinical signs and laboratory findings and the results compared with the findings of the urokinase pulmonary embolism trial. As far as history and clinical symptoms were concerned, breathlessness, chest pain, tachypnea, tachycardia and cyanosis were the dominating features. Among laboratory tests, the radiological and electrocardiographic findings of pulmonary hypertension were of little value. In contrast, arterial hypoxemia and isotope scanning provided the most reliable diagnostic information. The most frequent problem in differential diagnosis was acute myocardial infarction.
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PMID:[Diagnostic problems in acute pulmonary embolism]. 652

Pulmonary embolism is poorly diagnosed and therefore not treated in patients with chronic diseases, whereas it is overdiagnosed in formerly healthy patients. The diagnostic level is not satisfactory even in departments of cardiology. Insufficient use of auxiliary laboratory tests constitutes one of the main reasons for the unsatisfactory state of pulmonary embolism diagnostics. The clinical picture of pulmonary embolism depends on a) the size of pulmonary embolism, b) the previous state of the cardiopulmonary system. A massive pulmonary embolism can lead to a) sudden death, b) shock, c) acute cor pulmonale. The most typical diagnostic sign is suddenly developed or deteriorated dyspnea (present in 94% of patients). The presence of venous thrombosis and the appearance of sudden dyspnea always support the diagnosis very strongly. Dyspnea or tachypnea occur in more than 90% of patients. Dyspnea, tachypnea or deep venous thrombosis occur in 99% of patients with acute pulmonary embolism. Electrocardiographic signs of acute pulmonary embolism were present in 67% of our patients with hemodynamically significant pulmonary embolism. Electrocardiographic signs are most marked in cases in which pulmonary embolism originates suddenly, in patients with a normal cardiopulmonary system, if the pulmonary embolism is extensive and the electrocardiogram is carried out early and repeatedly. The electrocardiographic signs of pulmonary embolism in cardiac patients, however, are not specific and only rarely present. The principal advantages of the chest X-ray are simplicity, safety and low costs. A negative chest X-ray was found only in 16.6% of our patients with pulmonary embolism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The diagnosis of pulmonary embolism. 653 69

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.
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PMID:History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. 746 69

A 54-year-old man was hospitalized for a right renal tumor with intraluminal extension into the vena cava. He underwent radical nephrectomy with thrombectomy and regional lymphadenectomy. On the 8th postoperative day, he suddenly complained of dyspnea with tachypnea and cyanosis. Arterial blood gas analyses under an oxygen flow of 4L/min revealed PaO2 32.1 mmHg. Pulmonary angiography revealed filling defects in the right main pulmonary artery and left descending branch. Under the diagnosis of acute pulmonary embolism, thrombolytic and anti-coagulation therapy was performed and the patient recovered from the disease. We should be aware of pulmonary embolism as a postoperative complication of urological surgery.
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PMID:[Acute pulmonary embolism after radical operation for renal cell carcinoma with vena caval extension: a case cured by thrombolytic therapy]. 759 38


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