ABSTRACT
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.
ABSTRACT
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.
