Kristian Borup Wemmelund

Using Thoracic Ultrasonography to Accurately Assess Pneumothorax Progression During Positive Pressure Ventilation: A Comparison With CT Scanning

BACKGROUND Although thoracic ultrasonography accurately determines the size and extent of occult pneumothoraces (PTXs) in spontaneously breathing patients, there is uncertainty about patients receiving positive pressure ventilation. We compared the lung point (ie, the area where the collapsed lung still adheres to the inside of the chest wall) using the two modalities ultrasonography and CT scanning to determine whether ultrasonography can be used reliably to assess PTX progression in a positive-pressure-ventilated porcine model. METHODS Air was introduced in incremental steps into fi ve hemithoraces in three intubated porcine models. The lung point was identified on ultrasound imaging and referenced against the lateral limit of the intrapleural air space identified on the CT scans. The distance from the sternum to the lung point (S-LP) was measured on the CT scans and correlated to the insufflated air volume. RESULTS The mean total difference between the 131 ultrasound and CT scan lung points was 6.8 mm (SD, 7.1 mm; range, 0.0-29.3 mm). A mixed-model regression analysis showed a linear relationship between the S-LP distances and the PTX volume ( P , .001). CONCLUSIONS In an experimental porcine model, we found a linear relation between the PTX size and the lateral position of the lung point. The accuracy of thoracic ultrasonography for identifying the lung point (and, thus, the PTX extent) was comparable to that of CT imaging. These clinically relevant results suggest that ultrasonography may be safe and accurate in monitoring PTX progression during positive pressure ventilation.

Asphyxia causes ultrasonographic D-shaping of the left ventricle--an experimental porcine study.

In critical care, early diagnosis and correct treatment are of the utmost importance. Focused ultrasonography has gained acceptance as a pivotal tool for this by elucidating the underlying pathology. For example, massive pulmonary embolism is characterised by right ventricular dilatation. However, theoretically these characteristics might also be generated by asphyxia and the consequent hypoxia. We aimed to evaluate the ultrasonographic characteristics of asphyxia in a porcine model.

Dobutamine aggravates haemodynamic deterioration induced by pleural effusion: A randomised controlled porcine study

BACKGROUND Pleural effusion is a common finding in critically ill patients and may contribute to circulatory instability and the need for inotropic support. OBJECTIVE We hypothesised that dobutamine would affect the physiological determinants preload, afterload, contractility and changes of inferior vena cava characteristics during experimental pleural effusion. DESIGN A randomised, controlled laboratory study. SETTING Animal laboratory, conducted from March 2013 to May 2013. ANIMALS Twenty-four Landrace and Yorkshire female piglets (21.3 ± 1.7 kg). INTERVENTION Twenty piglets were included in the analyses. After inducing bilateral pleural effusion (30 ml kg−1), the piglets were block randomised to either incremental dobutamine infusion (n = 10) or control (n = 10). MAIN OUTCOME MEASURES Ultrasonographic measures of left ventricular end-diastolic area, left ventricular afterload, left ventricular fractional area change and inferior vena cava diameter and distensibility were used to assess the basic physiological effect of incremental dobutamine administration during experimental pleural effusion. RESULTS In the dobutamine group, preload, measured as left ventricular end-diastolic area, decreased from 11.3 ± 2.0 cm2 after creation of the pleural effusion to 8.1 ± 1.5 cm2 at a dobutamine infusion rate of 20 &mgr;g kg−1 min−1 (P < 0.001). In the same period, central venous pressure and the expiratory diameter of the inferior vena cava decreased from 9 ± 3 to 7 ± 4 mmHg (P < 0.001) and from 1.1 ± 0.2 to 0.9 ± 0.1 cm (P = 0.008), respectively. CONCLUSION In a porcine model of pleural effusion, dobutamine affected basic haemodynamic determinants substantially by decreasing left ventricular preload. Changes in central venous pressure and inferior vena cava characteristics were minimal, discouraging their use as indices of preload. This study underlines the significance of evaluating basic haemodynamic determinants to avoid inappropriate, potentially harmful treatment.

The intrapleural volume threshold for ultrasound detection of pneumothoraxes

Objectives Small pneumothoraxes (PTXs) may not impart an immediate threat to trauma patients after chest injuries. However, if these patients require positive pressure ventilation even a small amount of pleural air may be relevant. Point-of-care lung ultrasonography (US) is a reliable tool in the diagnosis of PTX, but the performance characteristics regarding detection of miniscule PTXs needs to be defined. We aimed at finding the volume threshold of intrapleural air where PTXs confidently can be diagnosed.

Effects of Progressive Hypoventilation on Left Ventricular Appearance: An Alternative Etiology of Acute Sonographic Short‐Axis D‐Shaping

The purpose of this study was to evaluate the effects of progressive hypoventilation on echocardiographic measures of the left ventricular (LV) appearance in a porcine model.

Dynamic ultrasound assessment of pneumothorax extension: a comparison with computer tomography

Methods Air was introduced into 5 hemithoraces (HTs) of 3 PPV porcine models. An anaesthesiologist experienced in US, identified LPs during the inspiratory phase and delineated the topography and extension of the PTX with subcutaneous needles. This was compared with the points where the lung detached from the inside of the chest wall identified by CT. The distance from sternum to the LP (S-LP) and PTX area were measured in two preset levels.

265: ESMOLOL IMPROVES CORONARY PERFUSION PRESSURE COMPARED TO EPINEPHRINE

Learning Objectives: Return of spontaneous circulation (ROSC) is dependent on coronary perfusion pressure (CPP), and epinephrine has been associated with an increased CPP. However, the β1-antagonistic effect of epinephrine may induce endocardial ischemia, leading to post ROSC myocardial dysfunction. This has led to experiments using the specific β1 antagonist esmolol during resuscitation. The isolated effect of esmolol on CPP has not yet been evaluated and therefore, we aimed to compare the effect of epinephrine, esmolol and placebo on CPP. Methods: 30 pigs were blindly randomized in a 1:1:1 ratio. Group 1 received epinephrine (20μg/kg 2mL dilution), Group 2 received esmolol(0.5mg/kg 2mL dilution) and Group 3 received placebo(2mL isotonic saline). VF was induced and after five minutes of untreated VF standard ALS compressions and ventilation were started. Medication was administered at the beginning of the 1st, 3rd, 5th, 7th and 9th cycle. Defibrillation attempts were included from the fourth cycle and onwards. Results: Seven piglets had ROSC, none in the epinephrine group, three in the esmolol group and four in the placebo group (p = 0.151). The peak CPP was 10 mmHg (3; 16), 10 mmHg (8; 16) and 12 mmHg (8; 12) in the epinephrine, esmololand placebo groups respectively (p = 0.168). After peaking, CPP declined in all groups to a nadir during the tenth cycle. The slope in the epinephrine group was significantly steeper compared to the esmolol group (p = 0.003).Conclusions: We found no difference in peak CPP between groups. CPP decreased at a higher rate in the epinephrine group compared to the esmolol group and thereby, esmolol improved CPP when compared to epinephrine during resuscitation. Furthermore, epinephrine did not increase the rate of ROSC. Esmolol has proven beneficial in all experimental studies reported including our and therefore we believe clinical trials of esmolol as a resuscitative drug are warranted.

160: VOLUME AND NOREPINEPHRINE RESTORE LEFT VENTRICULAR PRELOAD OTHERWISE DECREASED BY PLEURAL EFFUSION

Crit Care Med 2016 • Volume 44 • Number 12 (Suppl.) shock were identified. 15335 (14.2%) of these patients are obese. Obese group was younger and had a higher proportion of females. Acute myocardial infarction (MI) was co-existent in 46.4% hospitalizations with cardiogenic shock (42.2% in obese vs 47.1% among non-obese). Use of early revascularization (PCI or CABG in <24 hours from admission) and intra-aortic balloon pump (IABP) was slightly more common in obese patients, whereas, use of left ventricular assist device (LVAD) was slightly lower. The unadjusted mortality for obese patients was significantly lower than non-obese patients (32.5% vs 38.1%, p<0.001). The covariates for regression model included age category, gender, race, smoking, hospital characteristics, all Elixhauser co-morbidities, known coronary artery disease (CAD), atrial fibrillation, acute MI, use of LVAD, IABP, mechanical ventilation, and early revascularization. After adjusting for these variables, the odds ratio of in-hospital mortality among obese patients was 0.79 (95% CI 0.72 to 0.87, p<0.001). Conclusions: Among hospitalized patients with cardiogenic shock, obesity is associated with significantly lower risk-adjusted in-hospital mortality.