Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion.

BACKGROUND: Pleural effusion (PLE) may lead to low blood pressure and reduced cardiac output. Low blood pressure and reduced cardiac output are often treated with fluid loading and vasopressors. This study aimed to determine the impact of fluid loading and norepinephrine infusion on physiologic determinants of cardiac function obtained by ultrasonography during PLE. METHODS: In this randomised, blinded, controlled laboratory study, 30 piglets (21.9 ± 1.3 kg) had bilateral PLE (75 mL/kg) induced. Subsequently, the piglets were randomised to intervention as follows: fluid loading (80 mL/kg/h for 1.5 h, n = 12), norepinephrine infusion (0.01, 0.03, 0.05, 0.1, 0.2 and 0.3 µg/kg/min (15 min each, n = 12)) or control (n = 6). Main outcome was left ventricular preload measured as left ventricular end-diastolic area. Secondary endpoints included contractility and afterload as well as global measures of circulation. All endpoints were assessed with echocardiography and invasive pressure-flow measurements. RESULTS: PLE decreased left ventricular end-diastolic area, mean arterial pressure and cardiac output (p values < 0.001), but fluid loading (20 mL/kg) and norepinephrine infusion (0.05 µg/kg/min) restored these values (p values > 0.05) to baseline. Left ventricular contractility increased with norepinephrine infusion (p = 0.002), but was not affected by fluid loading (p = 0.903). Afterload increased in both active groups (p values > 0.001). Overall, inferior vena cava distensibility remained unchanged during intervention (p values ≥ 0.085). Evacuation of PLE caused numerical increases in left ventricular end-diastolic area, but only significantly so in controls (p = 0.006). CONCLUSIONS: PLE significantly reduced left ventricular preload. Both fluid and norepinephrine treatment reverted this effect and normalised global haemodynamic parameters. Inferior vena cava distensibility remained unchanged. The haemodynamic significance of PLE may be underestimated during fluid or norepinephrine administration, potentially masking the presence of PLE.

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

OBJECTIVES: 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. METHODS: Ten piglets were included in the experimental group, and 5 served as controls. The experimental group underwent 3 interventions of progressive hypoventilation (baseline: tidal volume, 240 mL; respiratory frequency, 16 minutes-1 ; first intervention: tidal volume, 240 mL; respiratory frequency, 8 minutes-1; second intervention: tidal volume, 240 mL; respiratory frequency, 4 minutes-1 ; and third intervention: tidal volume, 120 mL; respiratory frequency, 4 minutes-1 ). Respiratory resuscitation was initiated if the MAP decreased to 50% of the baseline level or at the end of the third intervention. Transthoracic sonography and invasive measurements were obtained throughout. The primary end point was the LV end-diastolic eccentricity index, a measure of LV D-shaping. RESULTS: The median LV end-diastolic eccentricity index increased from 1.1 (interquartile range, 1.0-1.1) at baseline to 1.4 (1.3-1.4) 3 minutes after the third intervention (P < .001) and returned to baseline after resuscitation (P = .093). The MAP declined from 87 mm Hg (81-92 mm Hg) to 50 mmHg (33-66 mm Hg) after initiation of the third intervention (P < .001). The mean pulmonary arterial pressure increased from 20 mm Hg (15-21 mm Hg) to 39 mm Hg (38-40 mm Hg) during the second intervention (P < .001). CONCLUSIONS: Progressive hypoventilation led to a marked D-configuration of the LV and a sharp decrease in systemic blood pressure. After respiratory resuscitation, sonographic measures normalized. These findings were explainable by the pressure changes observed within the left and right ventricles.

Effects of milrinone and epinephrine or dopamine on biventricular function and hemodynamics in right heart failure after pulmonary regurgitation.

Right ventricular failure (RVF) secondary to pulmonary regurgitation (PR) impairs right ventricular (RV) function and interrupts the interventricular relationship. There are few recommendations for the medical management of severe RVF after prolonged PR. PR was induced in 16 Danish landrace pigs by plication of the pulmonary valve leaflets. Twenty-three pigs served as controls. At reexamination the effect of milrinone, epinephrine, and dopamine was evaluated using biventricular conductance and pulmonary catheters. Seventy-nine days after PR was induced, RV end-diastolic volume index (EDVI) had increased by 33% (P = 0.006) and there was a severe decrease in the load-independent measurement of contractility (PRSW) (-58%; P = 0.003). Lower cardiac index (CI) (-28%; P < 0.0001), mean arterial pressure (-15%; P = 0.01) and mixed venous oxygen saturation (SvO2) (36%; P < 0.0001) were observed compared with the control group. The interventricular septum deviated toward the left ventricle (LV). Milrinone improved RV-PRSW and CI and maintained systemic pressure while reducing central venous pressure (CVP). Epinephrine and dopamine further improved biventricular PRSW and CI equally in a dose-dependent manner. Systemic and pulmonary pressures were higher in the dopamine-treated animals compared with epinephrine-treated animals. None of the treatments improved stroke volume index (SVI) despite increases in contractility. Strong correlation was detected between SVI and LV-EDVI, but not SVI and biventricular contractility. In RVF due to PR, milrinone significantly improved CI, SvO2, and CVP and increased contractility in the RV. Epinephrine and dopamine had equal inotropic effect, but a greater vasopressor effect was observed for dopamine. SV was unchanged due to inability of both treatments to increase LV-EDVI.

Effects of milrinone and epinephrine or dopamine on biventricular function and hemodynamics in an animal model with right ventricular failure after pulmonary artery banding.

Right ventricular (RV) failure due to chronic pressure overload is a main determinant of outcome in congenital heart disease. Medical management is challenging because not only contractility but also the interventricular relationship is important for increasing cardiac output. This study evaluated the effect of milrinone alone and in combination with epinephrine or dopamine on hemodynamics, ventricular performance, and the interventricular relationship. RV failure was induced in 21 Danish landrace pigs by pulmonary artery banding. After 10 wk, animals were reexamined using biventricular pressure-volume conductance catheters. The maximum pressure in the RV increased by 113% (P < 0.0001) and end-diastolic volume by 43% (P < 0.002), while left ventricular (LV) pressure simultaneously decreased (P = 0.006). Concomitantly, mean arterial pressure (MAP; -16%, P = 0.01), cardiac index (CI; -23%, P < 0.0001), and mixed venous oxygen saturation (SvO2 ; -40%, P < 0.0001) decreased. Milrinone increased CI (11%, P = 0.008) and heart rate (HR; 21%, P < 0.0001). Stroke volume index (SVI) decreased (7%, P = 0.03), although RV contractility was improved. The addition of either epinephrine or dopamine further increased CI and HR in a dose-dependent manner but without any significant differences between the two interventions. A more pronounced increase in biventricular contractility was observed in the dopamine-treated animals. LV volume was reduced in both the dopamine and epinephrine groups with increasing doses In the failing pressure overloaded RV, milrinone improved CI and increased contractility. Albeit additional dose-dependent effects of both epinephrine and dopamine on CI and contractility, neither of the interventions improved SVI due to reduced filling of the LV.

The intrapleural volume threshold for ultrasound detection of pneumothoraces: an experimental study on porcine models.

BACKGROUND: Small pneumothoraxes (PTXs) may not impart an immediate threat to trauma patients after chest injuries. However, the amount of pleural air may increase and become a concern for patients who require positive pressure ventilation or air ambulance transport. Lung ultrasonography (US) is a reliable tool in finding intrapleural air, but the performance characteristics regarding the detection of small PTXs need to be defined. The study aimed to define the volume threshold of intrapleural air when PTXs are accurately diagnosed with US and compare this volume with that for chest x-ray (CXR). METHODS: Air was insufflated into a unilateral pleural catheter in seven incremental steps (10, 25, 50, 100, 200, 350 and 500 mL) in 20 intubated porcine models, followed by a diagnostic evaluation with US and a supine anteroposterior CXR. The sonographers continued the US scanning until the PTXs could be ruled in, based on the pathognomonic US "lung point" sign. The corresponding threshold volume was noted. A senior radiologist interpreted the CXR images. RESULTS: The mean threshold volume to confirm the diagnosis of PTX using US was 18 mL (standard deviation of 13 mL). Sixty-five percent of the PTXs were already diagnosed at 10 mL of intrapleural air; 25%, at 25 mL; and the last 10%, at 50 mL. At an air volume of 50 mL, the radiologist only identified four out of 20 PTXs in the CXR pictures; i.e., a sensitivity of 20% (95% CI: 7%, 44%). The sensitivity of CXR increased as a function of volume but leveled off at 67%, leaving one-third (1/3) of the PTXs unidentified after 500 mL of insufflated air. CONCLUSION: Lung US is very accurate in diagnosing even small amounts of intrapleural air and should be performed by clinicians treating chest trauma patients when PTX is among the differential diagnoses.