Pulmonary Embolectomy

Embolectomy was carried out in eight patients with pulmonary emboli. Angiographic diagnosis was obtained in six, and in two cases pulmonary angiography could not be done because of the very critical condition of the patients. In the latter two, diagnosis was made based only on clinical findings. Two patients died in the operating room (25 percent). Six patients were discharged in good condition.It is emphasized that pulmonary embolectomy should be done in cases of pulmonary emboli when a clinical status of shock is present (systolic blood pressure less than 80 mm of mercury and the patient in low cardiac output syndrome) and when there is no response to medical treatment regardless of the degree of obstruction in the pulmonary arterial tree.     

Effects of emboli, positive-pressure ventilation, and airway water on lung water measurements

We tested the effects of microemboli, continuous positive-pressure ventilation (CPPV), and aspirated airway water on measurements of extravascular lung water by use of the technique of thermal indicator dilution (ETVL). A control group of dogs and a group of dogs in which dextran was infused created all levels of pulmonary edema. In an emboli group 0.125 g/kg of starch microemboli (63-74 micron diam) were infused. In groups with emboli and CPPV, starch emboli were infused and CPPV was then applied at 15 cmH2O. In an airway saline group measured amounts of saline were poured into the airway. In all groups postmortem pulmonary extravascular tissue weight (PETW) was determined and compared with the last ETVL. Emboli created an increased scatter when the last ETVL is compared with PETW because 1) blood trapped distal to emboli was included in the ETVL measurement, and/or 2) diffusion limitations for the thermal indicator were exceeded. Emboli and CPPV decreased ETVL/PETW. Airway saline (80 +/- 5%) was measured by ETVL. In conclusion, the ETVL technique is reliable in well-perfused lungs but loses accuracy in measuring lung water after emboli of any size or with large amounts of airway fluid.     

Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization

Brain compression with subdural air causes pulmonary hypertension and noncardiogenic pulmonary edema (A. B. Malik, J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 335-343, 1977). To see whether air emboli to the lungs rather than brain compression caused these findings, anesthetized dogs received intravenous air infusions, subdural air infusions, or brain compression from balloons inflated in the subdural space. Subdural air and intravenous air resulted in similar vascular responses. Pulmonary artery pressure (Ppa) increased 160% (P less than 0.01) and pulmonary venous pressure transiently rose 13 +/- 5 Torr (P less than 0.05) without an increase in left atrial pressure or cardiac output (Q). The end-tidal PCO2 fell 55% (P less than 0.01) and the postmortem weight of the lungs increased 55% (P less than 0.05). Brain compression with a subdural balloon instead of air only caused a 20% rise in Ppa and Q without pulmonary edema. Thus, pulmonary air emboli rather than brain compression accounts for the edema and pulmonary hypertension caused by subdural air. Catheters in pulmonary veins and the left atrium showed that air emboli cause transient pulmonary venous hypertension as well as a reproducible form of noncardiogenic pulmonary endema.     

Spatial distribution of venous gas emboli in the lungs.

The distribution of gaseous pulmonary emboli is presumed to be determined by their buoyancy. We hypothesized that regional pulmonary blood flow may also influence their distribution. Therefore, pulmonary blood flow was measured in supine, anesthetized dogs with use of 15-microm fluorescent microspheres at baseline and during N(2) embolism. The animals were killed, and the lungs were excised, air-dried, and diced into approximately 2-cm(3) pieces with weights and spatial coordinates recorded. Embolism was defined as a >10% flow decrease relative to baseline. Vertically, the incidence of embolism increased substantially by 6 +/- 1% per additional centimeter in height compared with baseline (P = 0.0003). Embolism also increased radially by 3 +/- 1%/cm from the hilum (P = 0.002). There was a weaker but statistically significant increase in embolism to pieces with greater baseline flow, 9 +/- 2% for every 1. 0 increase in relative baseline flow (P = 0.008). We conclude that the distribution of gaseous emboli is influenced by buoyancy and flow dynamics within the pulmonary vasculature.     

肺炎支原体肺炎伴喘息儿童血清25(OH)D_3、Th17/Treg表达水平与肺功能的关系

目的:探讨肺炎支原体肺炎伴喘息儿童血清25羟基维生素D3[25(OH)D_3]、辅助性17细胞/调节性T细胞(Th17/Treg)表达水平与肺功能的关系。方法:将新疆医科大学第五附属医院收治的肺炎支原体肺炎伴喘息患儿26例作为肺炎伴喘息组,肺炎支原体肺炎不伴有喘息患儿54例作为肺炎不伴喘息组,另选取健康儿童30例作为对照组,比较各组血清25(OH)D_3、白细胞介素(IL)-10、IL-17、Th17细胞及Treg细胞占CD4+T细胞比例及肺功能,并分析其相关性。结果:肺炎伴喘息组血清25(OH)D_3、IL-10、Treg细胞占CD4+T细胞比例低于肺炎不伴喘息组、对照组,Th17细胞占CD4+T细胞比例、Th17/Treg、IL-17高于肺炎不伴喘息组、对照组(P0.05)。各组第一秒最大呼气量占用力肺活量百分比(FEV1/FVC)比较差异无统计学意义(P0.05),肺炎伴喘息组FEV1占预计值百分比(FEV1%pred)、峰值呼气流量(PEF)低于肺炎不伴喘息组、对照组(P0.05),肺炎不伴喘息组与对照组FEV1%pred、PEF比较无统计学意义(P0.05)。肺炎伴喘息组患儿血清25 (OH)D_3与Th17/Treg、IL-17呈负相关(P0.05),与IL-10、FEV1%pred、PEF呈正相关(P0.05),血清Th17/Treg与IL-10、FEV1%pred、PEF呈负相关(P0.05),与IL-17呈正相关(P0.05)。结论:肺炎支原体肺炎伴喘息儿童血清25(OH)D_3、Th17/Treg表达水平异常,肺功能下降,且25(OH)D_3、Th17/Treg表达水平与肺功能相关。     

兔急性肺血栓栓塞模型建立及右心室压和心电图监测

目的建立操作简便,存活率高的急性肺动脉血栓栓塞（acute pulmonary thromboembolism,APTE）模型并监测右心室压及心电图,为研究肺栓塞（pulmonary embolism,PE）的病理生理及临床诊断治疗提供实验基础。方法兔麻醉后,经右侧颈总静脉插管至右心室观察正常右心室压。然后经此导管注入4个直径2 mm、长5 mm的长柱状自体血栓栓子建立兔急性PE模型。10只PE兔监测右心室压及心电图至栓塞后80 min。过量麻醉处死动物,取肺脏固定做病理检查。结果右心室导管的插管成功率92.45%,平均右心室正常压力（32.69±8.32）mmHg。PE模型的栓塞率100%,存活率87.76%。模型建立后右心室压平均增高（6.75±6.82）mmHg,51.35%出现异常心电图波形。结论1.兔正常右心室压为（32.69±8.32）mmHg。2.自体血栓栓子经颈静脉入口右心室注入法建立兔急性PE模型存活率高,右心室压可作为判断急性PE模型成功建立的指标。3.仅部分PE出现心电图异常,心电图异常不能作为判断兔PE的指标。     

Effect of pentosan polysulphate in minipigs with experimental pulmonary emboli

As a result of treatment with pentosan polysulphate in minipigs with experimental pulmonary emboli a decrease in mean pulmonary arterial pressure, an increase in blood flow of pulmonary artery and an increase in plasminogen activator was seen, compared with control animals who received saline infusion only.     

Venous occlusion measurement of pulmonary capillary pressure: effects of embolization

The effects of pulmonary arterial embolization on calculated pulmonary capillary pressure as determined by the venous occlusion technique are examined using a simple pressure-flow model for the lung. It is predicted that pulmonary, arterial embolization can induce significant underestimation of pulmonary capillary pressure in flowing vessels. This underestimation is related to the percent of vessels embolized and the caliber of pulmonary arteries that are embolized (i.e., the size of the emboli). Experimental verification of these theoretical findings is necessary before the conclusions can be extended to the interpretation of venous occlusion experiments in the lung.     

硫酸镁微量气泵吸入治疗毛细支气管炎患儿的疗效及对肺功能的影响

目的:探讨硫酸镁微量气泵吸入治疗毛细支气管炎患儿的疗效及对肺功能的影响。方法:选择2012年1月-2014年8月我院收治的毛细支气管炎患儿120例,随机分为研究组和对照组各60例。两组均给予吸氧、吸痰、镇静、止咳、抗感染和支气管扩张剂治疗,研究组再加用25%硫酸镁溶液0.1~0.2ml/(kg.次)气泵吸入治疗,比较两组临床疗效及患儿肺功能变化。结果:研究组总有效率为98.3%,显著高于对照组的88.3%(P0.05);研究组患儿咳嗽、气促、喘息、肺部哮鸣音/啰音消失时间及住院时间显著短于对照组(P0.05);治疗后两组患儿潮气量(VT)、达峰时间比(t PTEF/t E)和v PTEF/v E均明显升高,吸呼比(Ti/Te)明显降低(P0.05),研究组VT、t PTEF/t E和v PTEF/v E显著高于对照组,Ti/Te显著低于对照组(P0.05)。结论:硫酸镁微量气泵吸入治疗小儿毛细支气管炎可以改善患儿喘憋、气促、呼吸困难等症状以及肺功能,临床效果较好。     

Collaborative overview of randomised trials of antiplatelet therapy--III: Reduction in venous thrombosis and pulmonary embolism by antiplatelet prophylaxis among surgical and medical patients. Antiplatelet Trialists' Collaboration.

OBJECTIVE--To determine the efficacy of antiplatelet therapy as prophylaxis against deep venous thrombosis or pulmonary embolism in surgical and high risk medical patients. DESIGN--Overviews of all randomised trials of antiplatelet therapy that could have been available by March 1990 and in which deep venous thrombosis was assessed systematically. SETTING--53 trials (total 8400 patients) of an average of two weeks of antiplatelet therapy versus control in general or orthopaedic surgery; nine trials (600 patients) of antiplatelet therapy versus control in other types of immobility; 18 trials (1000 patients) of one antiplatelet regimen versus another. RESULTS--Overall, a few weeks of antiplatelet therapy produced a highly significant (2P < 0.00001) reduction in deep venous thrombosis. 25% of patients allocated antiplatelet therapy versus 34% of appropriately adjusted controls had deep venous thrombosis detected by systematic fibrinogen scanning or venography, representing prevention in about 90 patients per 1000 allocated antiplatelet therapy. There was an even greater proportional reduction in pulmonary embolism: such emboli were detected among 47 (1.0%) antiplatelet allocated patients versus an adjusted control total of 129 (2.7%), representing prevention among about 17 patients per 1000 treated (2P < 0.00001). In analyses confined to surgical trials, the proportional reductions were similar and separately significant for nonfatal pulmonary embolism (0.7% antiplatelet therapy v 1.8% control; 2P < 0.00001) and for deaths attributed to pulmonary embolism (0.2% v 0.9%; 2P = 0.0001). There was a slight but non-significant excess of deaths from other causes (1.0% v 0.7%), which made the difference in total mortality nonsignificant, though still favourable (1.2% v 1.5%). Information on adding antiplatelet therapy to heparin was limited but, at least for pulmonary embolism, suggested more protection from the combination than from heparin alone. The proportional reduction in the odds of suffering a deep venous thrombosis was roughly the same in patients having general surgery, traumatic orthopaedic surgery, and elective orthopaedic surgery (and in medical patients who were at increased risk of thromboembolism). For pulmonary embolism the numbers affected were smaller, but again the reductions were highly significant both in general surgery (16 (0.5%) v 58 (1.7%) pulmonary emboli; 2P < 0.0001) and in orthopaedic surgery (28 (2.7%) v 63 (6.1%) pulmonary emboli; 2P < 0.0002). CONCLUSION--It had previously been supposed that antiplatelet therapy did not influence venous thromboembolism, and many surgeons and physicians do not use it routinely for thromboprophylaxis, even for patients who are at substantial risk of deep venous thrombosis or pulmonary embolism. These results indicate that antiplatelet therapy--either alone or, for greater effect, in addition to other proved forms of thromboprophylaxis (such as subcutaneous heparin)--should be considered.     

Effect of ventilation with soluble and diffusible gases on the size of air emboli

Pulmonary hypertension resulting from venous air embolism is known to increase after ventilation with highly soluble and diffusible gases. Exacerbation of the hypertension could be due to further blockage of the circulation if the bubbles enlarge as a result of ingress of gas by diffusion. This mechanism has been frequently cited but lacks direct proof. To determine directly whether intravascular air bubbles actually enlarge when highly soluble and diffusible gases are inspired, we used microscopy to measure the size of gas emboli in vivo. When air bubbles were injected into the right atrium, the bubbles that appeared in pulmonary arterioles were larger during ventilation with helium or nitrous oxide than with air. Air bubbles injected into the pulmonary artery enlarged when the inspired gas was changed to helium or nitrous oxide. The direction, magnitude, and timing of changes in bubble size were consistent with a net diffusion of gas into the bubbles. These data support the idea that venous air emboli enlarge during ventilation with soluble and diffusible gases and thereby cause further vascular obstruction.     

Acute postembolic pulmonary edema in vagotomized rats

1. In the rat, pulmonary embolism induced by intravenous administration of gaseous carbon dioxide increases intrapulmonary water content. When the rat is vagotomized before emboli are produced, an important lung edema is found. 2. Strong respiratory stimulation with lung hyperinflation seems to be the cause of this facilitated alveolar transudation. 3. Mechanical factors operating after pulmonary embolism are those which explain transudation after inhalation of hypercapnic gas mixtures in vagotomized rats.     

Respiratory mechanics in men following a deep air dive

The mechanical properties of the lungs were measured in 10 men before and after a simulated air dive to 285 ft of seawater (87 m). The objective was to determine whether a dive likely to produce pulmonary bubble emboli would alter lung mechanics. Lung function was measured predive and at 1, 2, 3, 6, 7, and 23 h postdive. Measurements of lung function were also made at identical times on a control day when no dive was made. Each set of measurements included precordial Doppler signals, pulmonary resistance, quasistatic lung compliance, forced vital capacity (FVC), forced expired volume after 1.0 s (FEV 1.0), the ratio of FEV 1.0 to FVC (FEV 1.0/FVC%), and maximal airflow after 50 and 75% of the vital capacity had been expired (Vmax50 and Vmax75, respectively). Base-line measurements of pulmonary resistance and quasistatic compliance were normal in all subjects. FVC and FEV 1.0 were greater than predicted for most subjects and were increased proportionately so that the FEV 1.0/FVC% was normal. Following the dive, bubble signals were heard in four subjects, and two subjects had mild symptoms of decompression sickness. No subject demonstrated any alteration in lung function that could be attributed to the dive. We concluded that stressful decompressions capable of producing "silent" pulmonary bubble emboli do not alter lung mechanics.     

Experimental crystal violet and methyl violet poisoning in dogs and cattle

Crystal violet has been observed to cause fatal pulmonary alterations in dogs. To further evaluate this toxicity and the toxicity of methyl violet, 12 dogs and 2 calves were given 1 percent aqueous solutions of the dyes intravenously. Both dyes caused the formation of numerous dye protein emboli which lodged in the lungs producing thrombosis and infarction. A 1 per cent solution of the dyes caused precipitate formation when added to bovine serum or heparinized plasma IN VITRO. Serum proteins in general were decreased as determined by paper electrophoresis of serumcrystal violet supernatants. These dyes could be used effectively in studying the pathogenesis of certain pulmonary lesions, especially emphysema and alveolar epithelial hyperplasia.     

Relationship between bronchial hyperresponsiveness and impaired lung function after infantile asthma

Wheezing during infancy has been linked to early loss of pulmonary function. We prospectively investigated the relation between bronchial hyperresponsiveness (BHR) and progressive impairment of pulmonary function in a cohort of asthmatic infants followed until age 9 years. We studied 129 infants who had had at least three episodes of wheezing. Physical examinations, baseline lung function tests and methacholine challenge tests were scheduled at ages 16 months and 5, 7 and 9 years. Eighty-three children completed follow-up. Twenty-four (29%) infants had wheezing that persisted at 9 years of age. Clinical outcome at age 9 years was significantly predicted by symptoms at 5 years of age and by parental atopy. Specific airway resistance (sRaw) was altered in persistent wheezers as early as 5 years of age, and did not change thereafter. Ninety-five per cent of the children still responded to methacholine at the end of follow-up. The degree of BHR at 9 years was significantly related to current clinical status, baseline lung function, and parental atopy. BHR at 16 months and 5 years of age did not predict persistent wheezing between 5 and 9 years of age, or the final degree of BHR, but it did predict altered lung function. Wheezing that persists from infancy to 9 years of age is associated with BHR and to impaired lung function. BHR itself is predictive of impaired lung function in children, strongly pointing to early airway remodeling in infantile asthma.     

Prophylactic Anticoagulant Therapy against Pulmonary Emboli in Acute Paraplegia

Prophylactic anticoagulant therapy within a few days of admitting a patient with a spinal injury appears to offer advantages in preventing pulmonary emboli. It was not found to hinder the patient''s management.     

Modeling of massive embolism of the pulmonary artery in experimental animals

In anesthesized dogs with closed chest and natural respiration massive embolism of pulmonary artery has been simulated with the aid of marked muscular emboli. In 6 h after massive pulmonary embolism pressure in the lesser circulation somewhat decreased, however, it was higher than the initial and control data.     

Takotsubo syndrome with pulmonary embolism: a case report and literature review

Background

Takotsubo syndrome (TTS) is an acute cardiac condition with reversible heart failure which is often triggered by psychological and physical stressful events. Although pulmonary embolism (PE) was reported as a trigger for TTS, the concurrence of TTS and PE has been rarely reported, let alone that triggered by PE. Here we describe a case of a postmenopausal female presenting with symptoms similar to myocardial ischemia, which may be caused by PE, and review the available literature that may help clinicians with their practice to similar situations since no published guidelines are available.

Case presentation

An 86-year-old female was referred to the emergency department for unrelieved chest tightness, shortness of breath and back pain. Cardiac biomarkers were mildly elevated and electrocardiogram displayed pathologic Q-waves, ST-segment elevation and inverted T-waves. Unexpectedly, coronary angiography was in absence of obstructed coronary atherosclerosis or acute plaque rupture. Chest computed tomography illustrated multiple pulmonary emboli in bilateral pulmonary arteries. She had suffered from long-term right lower extremity pain and experienced a long railway journey with less activity. Both echocardiogram and cardiac magnetic resonance demonstrated regional hypokinesia of left ventricle. She received anticoagulant and diuretic therapies, three-month follow up after discharge revealed uneventful recovery without any pulmonary emboli or regional motion abnormalities, thus she was retrospectively diagnosed with TTS caused by PE.

Conclusion

TTS and PE are scarcely concurrent and PE can exert as a potential trigger for TTS. TTS is easily misdiagnosed, actively seeking possible risk factors of TTS is in favor of early diagnosis and timely intervention. TTS with PE is reversible, timely and effective treatments ensure the best possible outcome.

     

Indications for Vena Caval Fenestration

A retrospective study of 20 patients who underwent vena caval fenestration showed that in 50% of the patients the procedure was done for prophylaxis and in 50% it was done for therapeutic reasons. After this procedure five patients had persistent leg swelling, two had deep venous thrombosis, two had pulmonary emboli and one died of a respiratory arrest. We recommend limiting the use of vena caval fenestration to those patients who have verified pulmonary embolism while adequately anticoagulated or patients who have pulmonary embolism and a major contraindication to anticoagulation.     

Pulmonary Function in Infants with Swallowing Dysfunction

BackgroundSwallowing dysfunction can lead to recurring aspiration and is frequently associated with chronic symptoms such as cough and wheezing in infants. Our objective was to describe the characteristics of infants with swallowing dysfunction, determine if pulmonary function abnormalities are detectable, and if they improve after therapy.MethodsWe studied 38 infants with a history of coughing and wheezing who had pulmonary function tests performed within two weeks of their diagnosis of swallowing dysfunction. The raised lung volume rapid thoracoabdominal compression technique was used. After 6 months of therapy, 17 of the infants repeated the tests.ResultsInitially, 25 had abnormal spirometry, 18 had abnormal plethysmography, and 15 demonstrated bronchodilator responsiveness. Six months later test were repeated for seventeen patients. Ten patients had continued abnormal spirometry, two patients remained normal, three patients’ abnormal spirometry had normalized, and two patients’ previously normal studies became abnormal. Eight of the 17 patients had continued abnormal plethysmography, six had continued normal plethysmography, and three patients’ normal plethysmography became abnormal. After 6 months of treatment, eight patients demonstrated bronchodilator responsiveness, of which five continued to demonstrate bronchodilator responsiveness and three developed responsiveness. The remainder either continued to be non- bronchodilator responsive (two) or lost responsiveness (three.) The findings of the abnormal tests in most infants tested is complicated by frequent occurrence of other co-morbidities in this population, including gastroesophageal reflux in 23 and passive smoke exposure in 13 of the infants.ConclusionsThe interpretation of lung function changes is complicated by the frequent association of swallowing dysfunction with gastroesophageal reflux and passive smoke exposure in this population. Six months of medical therapy for swallowing dysfunction/gastroesophageal reflux did not significantly improve pulmonary function in these infants. Long-term studies will be necessary to determine which of these changes persists into adulthood.