The effect of open lung ventilation on right ventricular and left ventricular function in lung-lavaged pigs.

INTRODUCTION: Ventilation according to the open lung concept (OLC) consists of recruitment maneuvers, followed by low tidal volume and high positive end-expiratory pressure, aiming at minimizing atelectasis. The minimization of atelectasis reduces the right ventricular (RV) afterload, but the increased intrathoracic pressures used by OLC ventilation could increase the RV afterload. We hypothesize that when atelectasis is minimized by OLC ventilation, cardiac function is not affected despite the higher mean airway pressure. METHODS: After repeated lung lavage, each pig (n = 10) was conventionally ventilated and was ventilated according to OLC in a randomized cross-over setting. Conventional mechanical ventilation (CMV) consisted of volume-controlled ventilation with 5 cmH2O positive end-expiratory pressure and a tidal volume of 8-10 ml/kg. No recruitment maneuvers were performed. During OLC ventilation, recruitment maneuvers were applied until PaO2/FiO2 > 60 kPa. The peak inspiratory pressure was set to obtain a tidal volume of 6-8 ml/kg. The cardiac output (CO), the RV preload, the contractility and the afterload were measured with a volumetric pulmonary artery catheter. A high-resolution computed tomography scan measured the whole lung density and left ventricular (LV) volumes. RESULTS: The RV end-systolic pressure-volume relationship, representing RV afterload, during steady-state OLC ventilation (2.7 +/- 1.2 mmHg/ml) was not significantly different compared with CMV (3.6 +/- 2.5 mmHg/ml). Pulmonary vascular resistance (OLC, 137 +/- 49 dynes/s/cm5 versus CMV, 130 +/- 34 dynes/s/cm5) was comparable between groups. OLC led to a significantly lower amount of atelectasis (13 +/- 2% of the lung area) compared with CMV (52 +/- 3% of the lung area). Atelectasis was not correlated with pulmonary vascular resistance or end-systolic pressure-volume relationship. The LV contractility and afterload during OLC was not significantly different compared with CMV. Compared with baseline, the LV end-diastolic volume (66 +/- 4 ml) decreased significantly during OLC (56 +/- 5 ml) ventilation and not during CMV (61 +/- 3 ml). Also, CO was significantly lower during OLC ventilation (OLC, 4.1 +/- 0.3 l/minute versus CMV, 4.9 +/- 0.3 l/minute). CONCLUSION: In this experimental study, OLC resulted in significantly improved lung aeration. Despite the use of elevated airway pressures, no evidence was found for a negative effect of OLC on RV afterload or LV afterload, which might be associated with a loss of hypoxic pulmonary vasoconstriction due to alveolar recruitment. The reductions in the CO and in the mean pulmonary artery pressure were consequences of a reduced preload.

Assessment of right ventricular fibrosis in different forms of pulmonary atresia with ventricular septal defect.

BACKGROUND: In pulmonary atresia with ventricular septal defect (PA-VSD), the corrective surgical strategy aims to reduce the right ventricular (RV) overload and restore physiological pulmonary perfusion before the characteristic RV hypertrophy and fibrosis become irreversible. OBJECTIVE: To assess RV fibrosis in different forms of PA-VSD. METHODS: RV biopsies were obtained at corrective surgery from PA-VSD patients (n=14, mean age 2.5+/-1.2 years) with patent arterial duct (PAD group, n=6; mean age 1.7+/-0.5 years) or systemic-pulmonary collateral arteries (SPCA group, n=8; mean age 3.2+/-1.2 years) and from age-matched controls (control group, n=6; mean age 2.5+/-1.8 years). Myocardial expression patterns (messenger RNA [mRNA] and protein levels) of the extracellular matrix proteins (eg, fibronectin and collagens [subtype I alpha and III) were quantitatively analyzed in relation to myocardial cell hypertrophy. RESULTS: Comparing the age of PA-VSD patients at surgery, the SPCA group was older than the PAD group (P=0.01). Expression analysis by reverse transcriptase polymerase chain reaction showed significantly higher mRNA levels in patients with PA-VSD for collagen III (PA-VSD versus controls; 0.9+/-0.2 versus 0.6+/-0.1, P=0.03) than in controls, whereas collagen I alpha and fibronectin mRNA levels did not differ. No differences were found between the PAD and SPCA groups. The myocyte cross sectional surface area showed enhanced myocyte hypertrophy in patients with PA-VSD compared with the control group (P=0.015), with no significant difference between the PAD and SPCA groups. Video image analysis of immunohistochemical staining corrected for hypertrophy revealed unchanged interstitial collagens and fibronectin levels in all groups. However, perivascular staining corrected for the vessel lumen area showed significantly lower total collagen levels in patients with PA-VSD than in the control group (3.2+/-1.2 versus 7.2+/-2.8, respectively; P=0.004). CONCLUSIONS: The results indicate that the extracellular matrix support for the coronary blood vessels appears to be suboptimal in patients with PA-VSD. The staged surgical approach in the SPCA group (with a higher age at correction) did not result in an excessive accumulation of fibrosis markers in the RV myocardium.

[Fatal respiratory failure in a morbidly obese patient]. / Respiratoire insufficiëntie met een fataal beloop bij een patiënt met morbide obesitas.

BACKGROUND: Healthcare professionals are seeing an increasing number of morbidly obese patients. Medical interventions are often difficult to perform in these patients. In acute situations this can lead to major problems. CASE DESCRIPTION: Assistance from a mobile medical team was requested for a 42-year-old male weighing 350 kg with severe respiratory failure. Transporting the patient was problematic due to his build. The hospital to which he was brought after hours of delay lacked the appropriate space and resources for morbidly obese patients. Since the condition of the patient deteriorated, intubation and mechanical ventilation were required. Despite additional equipments for problematic airway access, the procedure failed and the patient died due to respiratory failure. CONCLUSION: Designating centres for care, also in the acute situations, of morbidly obese patients is recommended, to improve the care of these patients and to prevent disasters.

Anaesthesiological and ventilatory precautions during cardiac surgery in Steinert's disease.

Myotonic dystrophia type I or Steinert's disease is a progressive multisystemic-inherited neuromuscular disease. Higher sensitivity to sedatives, anaesthetic, and neuromuscular blocking agents may result in cardiovascular and respiratory complications. We describe the anaesthesiological and ventilatory measures in a 43-year-old patient with Steinert's disease successfully undergoing cardiac surgery.

Open lung ventilation does not increase right ventricular outflow impedance: An echo-Doppler study.

OBJECTIVE: Ventilation according to the open lung concept (OLC) consists of recruitment maneuvers, followed by low tidal volume and elevated positive end-expiratory pressure (PEEP). Elevated PEEP is associated with an increased right ventricular afterload. We investigated the effect of OLC ventilation on right ventricular outflow impedance during inspiration and expiration in patients after cardiac surgery using transesophageal echo-Doppler. DESIGN: A prospective, single-center, crossover, randomized, controlled clinical study. SETTING: Cardiothoracic intensive care unit of a university hospital. PATIENTS: Twenty-eight patients scheduled for elective cardiac surgery with cardiopulmonary bypass. INTERVENTIONS: In the intensive care unit, each patient was ventilated for approximately 30 mins according to both OLC and conventional ventilation. During OLC ventilation, recruitment maneuvers were applied until PaO2/FiO2 was >375 torr (50 kPa); during conventional ventilation no recruitment maneuvers were performed. MEASUREMENTS AND MAIN RESULTS: Transesophageal echo-Doppler measurements were performed at end-inspiration and end-expiration in a steady-state condition, 20 mins after initiation of a ventilation strategy. Mean acceleration of flow was determined in the long axis of the pulmonary artery in a transverse axis view. During OLC ventilation, a total PEEP of 14 +/- 4 cm H2O was applied vs. 5 cm H2O during conventional ventilation. Mean acceleration during expiration was comparable between groups. During inspiration, OLC ventilation did not cause a decrease of mean acceleration compared with expiration, whereas this did occur during conventional ventilation. CONCLUSIONS: Despite the use of elevated PEEP levels, ventilation according to OLC does not change right ventricular outflow impedance during expiration and decreases right ventricular outflow impedance during inspiration.

Right ventricular collagen and fibronectin levels in patients with pulmonary atresia and ventricular septal defect.

Pulmonary atresia (PA) with ventricular septal defect (VSD) is an extreme form of tetralogy of Fallot with characteristic right ventricular hypertrophy. To reduce the right ventricular overload, these children have to undergo staged corrective surgery to restore physiological pulmonary perfusion. We studied the degree of fibrosis by analysing the myocardial expression pattern (at mRNA and protein level) of the extracellular matrix proteins, collagen and fibronectin in biopsies taken at corrective surgery from 14 patients affected by PA,VSD. Expression analysis by RT-PCR showed significantly higher levels for collagen III (p = 0.03), whereas collagen Ialpha (p = 0.31) and fibronectin (p = 0.47) mRNA levels remained unaltered in PA, VSD patients as compared to age matched controls. Video image analysis of immunohistochemical staining showed unchanged interstitial levels for total collagen (p = 0.17) as well as for fibronectin (p = 0.13) in the patients with PA, VSD. However, peri-vascular staining for collagen (p < 0.01) and fibronectin (p = 0.02) represented as the peri-vascular stained area corrected for the vessel lumen area showed significantly decreased levels in the PA, VSD group as compared to controls. Our results indicate that the patients with PA, VSD have inadequate extracellular matrix support for their coronary blood vessels and perhaps due to an altered biosynthesis of collagen and fibronectin network.