Embolia pulmonar quase fatal, um modelo experimental

Pereira, Daniel José Rocha; Moreira, Marcos Mello; Paschoal, Ilma Aparecida; Martins, Luiz Ferreira; Metze, Konradin; Moreno, Heitor

doi:10.5935/1678-9741.20110023

Cited by 12 publications

(6 citation statements)

References 23 publications

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“…A number of experimental model studies have demonstrated that PaCO 2 does not vary in near-fatal PE. [ 29 ] In the present study, PetCO 2 had a high negative predictive value in excluding PE. [ 30 ] In the diagnosis of high-risk PE, a decrease in PetCO 2 was suggested to be an earlier detection of intraoperative pulmonary emboli.…”

Section: Discussionsupporting

confidence: 51%

Study of Cardiac Arrest Caused by Acute Pulmonary Thromboembolism and Thrombolytic Resuscitation in a Porcine Model

Zhao

Liu

Yang

et al. 2016

Chinese Medical Journal

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Background:The success rate of resuscitation in cardiac arrest (CA) caused by pulmonary thromboembolism (PTE) is low. Furthermore, there are no large animal models that simulate clinical CA. The aim of this study was to establish a porcine CA model caused by PTE and to investigate the pathophysiology of CA and postresuscitation.Methods:This model was induced in castrated male pigs (30 ± 2 kg; n = 21) by injecting thrombi (10–15 ml) via the left external jugular vein. Computed tomographic pulmonary angiography (CTPA) was performed at baseline, CA, and return of spontaneous circulation (ROSC). After CTPA during CA, cardiopulmonary resuscitation (CPR) with thrombolysis (recombinant tissue plasminogen activator 50 mg) was initiated. Hemodynamic, respiratory, and blood gas data were monitored. Cardiac troponins T, cardiac troponin I, creatine kinase-MB, myoglobin, and brain natriuretic peptide (BNP) were measured by enzyme-linked immunosorbent assay. Data were compared between baseline and CA with paired-sample t-test and compared among different time points for survival animals with repeated measures analysis of variance.Results:Seventeen animals achieved CA after emboli injection, while four achieved CA after 5–8 ml more thrombi. Nine animals survived 6 h after CPR. CTPA showed obstruction of the pulmonary arteries. Mean aortic pressure data showed occurrence of CA caused by PTE (Z = −2.803, P = 0.002). The maximal rate of mean increase of left ventricular pressure (dp/dtmax) was statistically decreased (t = 6.315, P = 0.000, variation coefficient = 0.25), and end-tidal carbon dioxide partial pressure (PetCO2) decreased to the lowest value (t = 27.240, P = 0.000). After ROSC (n = 9), heart rate (HR) and mean right ventricular pressure (MRVP) remained different versus baseline until 2 h after ROSC (HR, P = 0.036; MRVP, P = 0.027). Myoglobin was statistically increased from CA to 1 h after ROSC (P = 0.036, 0.026, 0.009, respectively), and BNP was increased from 2 h to 6 h after ROSC (P = 0.012, 0.014, 0.039, respectively).Conclusions:We established a porcine model of CA caused by PTE. The dp/dtmax and PetCO2 may be important for the occurrence of CA, while MRVP may be more important in postresuscitation.

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Section: Discussionsupporting

confidence: 51%

Study of Cardiac Arrest Caused by Acute Pulmonary Thromboembolism and Thrombolytic Resuscitation in a Porcine Model

Zhao

Liu

Yang

et al. 2016

Chinese Medical Journal

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“…It has the same shape of the other gas elimination curves, with the advantage of being obtained with a gas which is normally produced in the body and eliminated by the lungs. 11 , 12 The main variables analyzed were end-tidal concentration of carbon dioxide (ETCO 2 ), Slope of phase 2 (Slp2), and Slope of phase 3 (Slp3) of capnogram. Slp2 represents the rapid increase in CO 2 coming from short paths to alveoli; it comes immediately after the elimination of the air from the dead space.…”

Section: Introductionmentioning

confidence: 99%

COPD phenotypes on computed tomography and its correlation with selected lung function variables in severe patients

Silva¹,

Paschoal²,

Capitani³

et al. 2016

COPD

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BackgroundComputed tomography (CT) phenotypic characterization helps in understanding the clinical diversity of chronic obstructive pulmonary disease (COPD) patients, but its clinical relevance and its relationship with functional features are not clarified. Volumetric capnography (VC) uses the principle of gas washout and analyzes the pattern of CO2 elimination as a function of expired volume. The main variables analyzed were end-tidal concentration of carbon dioxide (ETCO2), Slope of phase 2 (Slp2), and Slope of phase 3 (Slp3) of capnogram, the curve which represents the total amount of CO2 eliminated by the lungs during each breath.ObjectiveTo investigate, in a group of patients with severe COPD, if the phenotypic analysis by CT could identify different subsets of patients, and if there was an association of CT findings and functional variables.Subjects and methodsSixty-five patients with COPD Gold III–IV were admitted for clinical evaluation, high-resolution CT, and functional evaluation (spirometry, 6-minute walk test [6MWT], and VC). The presence and profusion of tomography findings were evaluated, and later, the patients were identified as having emphysema (EMP) or airway disease (AWD) phenotype. EMP and AWD groups were compared; tomography findings scores were evaluated versus spirometric, 6MWT, and VC variables.ResultsBronchiectasis was found in 33.8% and peribronchial thickening in 69.2% of the 65 patients. Structural findings of airways had no significant correlation with spirometric variables. Air trapping and EMP were strongly correlated with VC variables, but in opposite directions. There was some overlap between the EMP and AWD groups, but EMP patients had signicantly lower body mass index, worse obstruction, and shorter walked distance on 6MWT. Concerning VC, EMP patients had signicantly lower ETCO2, Slp2 and Slp3. Increases in Slp3 characterize heterogeneous involvement of the distal air spaces, as in AWD.ConclusionVisual assessment and phenotyping of CT in COPD patients is feasible and may help identify functional and clinically different subsets of patients. VC may provide useful information about the heterogeneous involvement of lung structures in COPD.

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“…There are overall very few in vivo models of acute PE and, to our knowledge, none that fulfills all of the criteria above. 14 – 22 …”

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confidence: 99%

A porcine in‐vivo model of acute pulmonary embolism

et al. 2017

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Acute pulmonary embolism (PE) is the third most common cardiovascular cause of death after acute myocardial infarction and stroke. Patients are, however, often under-treated due to the risks associated with systemic thrombolysis and surgical embolectomy. Novel pharmacological and catheter-based treatment strategies show promise, but the data supporting their use in patients are sparse. We therefore aimed to develop an in vivo model of acute PE enabling controlled evaluations of efficacy and safety of novel therapies. Danish Landrace pigs (n = 8) were anaesthetized and mechanically ventilated. Two pre-formed autologous PEs (PE1, PE2, 20 × 1 cm) were administered consecutively via the right external jugular vein. The intact nature and central location were visualized in situ by magnetic resonance imaging (MRI). The hemodynamic and biochemical responses were evaluated at baseline (BL) and after each PE by invasive pressure measurements, MRI, plus arterial and venous blood analysis. Pulmonary arterial pressure increased after administration of the PEs (BL: 16.3 ± 1.2, PE1: 27.6 ± 2.9, PE2: 31.6 ± 3.1 mmHg, BL vs. PE1: P = 0.0027, PE1 vs. PE2: P = 0.22). Animals showed signs of right ventricular strain evident by increased end systolic volume (BL: 60.9 ± 5.1, PE1: 83.3 ± 5.0, PE2: 99.4 ± 6.5 mL, BL vs. PE1: P = 0.0005, PE1 vs. PE2: P = 0.0045) and increased plasma levels of Troponin T. Ejection fraction decreased (BL: 58.9 ± 2.4, PE1: 46.4 ± 2.9, PE2: 37.3 ± 3.5%, BL vs. PE1: p = 0.0008, PE1 vs. PE2: P = 0.009) with a compensatory increase in heart rate preserving cardiac output and systemic blood pressure. The hemodynamic and biochemical responses were comparable to that of patients suffering from intermediate-high-risk PE. This porcine model mirrors the anatomical and physiologic changes seen in human patients with intermediate-high-risk PE, and may enable testing of future therapies for this disease.

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Embolia pulmonar quase fatal, um modelo experimental

Cited by 12 publications

References 23 publications

Study of Cardiac Arrest Caused by Acute Pulmonary Thromboembolism and Thrombolytic Resuscitation in a Porcine Model

Study of Cardiac Arrest Caused by Acute Pulmonary Thromboembolism and Thrombolytic Resuscitation in a Porcine Model

COPD phenotypes on computed tomography and its correlation with selected lung function variables in severe patients

A porcine in‐vivo model of acute pulmonary embolism

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