Drago Dacar

Minimally invasive versus conventional aortic valve operations: a prospective study in 120 patients

BACKGROUND Risk evaluation comparing the minimally invasive and standard aortic valve operations has not been studied. METHODS Four surgeons were randomly assigned to perform the minimally invasive (L-shaped sternotomy) (group 1) or the conventional (group 2) operation in 120 patients exclusively. RESULTS In both groups (n = 60) a CarboMedics prothesis was implanted in 90% of patients. There was no significant difference in the cross-clamping period (group 1, 60 minutes; range, 35 to 116 minutes), in the duration of extracorporal circulation (group 1, 84 minutes; range, 51 to 179 minutes) or in the time from skin-to-skin (group 1, 195 minutes; range, 145 to 466 minutes). Patients in group 1 were extubated earlier (p<0.001), the postoperative blood loss was less (p<0.001), and the need for analgesics was reduced (p<0.05). In 5 patients in group 1 a redo operation was required for bleeding (p>0.05), 3 patients in group 1 required a redo operation because of paravalvular leakage or endocarditis (p>0.05), the 30-day mortality rate was 1.6%. Overall the survival rate was 95% in group 1 and 97% in group 2 (mean follow-up, 294 days; range, 30 to 745 days). CONCLUSION The advantages of minimally invasive aortic valve operation include reduced trauma from incision and duration of ventilation, decreased blood loss and postoperative pain, the avoidance of groin cannulation, and a cosmetically attractive result. Simple equipment is used with a high degree of effectiveness and with no sacrifice of safety. Our study demonstrated the practicability and reliability of this new method.

Inhaled nitric oxide in patients with critical pulmonary perfusion after fontan-type procedures and bidirectional glenn anastomosis

OBJECTIVE The aim of this study was to evaluate the effects of inhaled nitric oxide in patients with critical pulmonary perfusion after Fontan-type procedures and bidirectional Glenn anastomosis. METHODS Inhaled nitric oxide (mean 4.1 +/- 0.7 ppm, 1.5 to 10 ppm) was administered in 13 patients (mean age 5.6 +/- 1.6 years, 1.5 to 17 years) with critical pulmonary perfusion (central venous pressure > 20 mm Hg or transpulmonary pressure gradient > 10 mm Hg) in the early postoperative period after total cavopulmonary connection (n = 9) or after bidirectional Glenn anastomosis (n = 4). RESULTS In patients after total cavopulmonary connection inhaled nitric oxide therapy decreased central venous pressure by 15.3% +/- 1.4% (p = 0.0001) and transpulmonary pressure gradient by 42% +/- 8% (p = 0.0008) and increased mean systemic arterial and left atrial pressures by 12% +/- 3.6% (p = 0.011) and 28% +/- 8% (p = 0.007), respectively. Arterial and venous oxygen saturations improved by 8.2% +/- 1% (p = 0.005) and 14% +/- 4.3% (p = 0.03), respectively. In patients after bidirectional Glenn anastomosis inhaled nitric oxide therapy resulted in a decrease of central venous pressure by 22% +/- 1% and of the transpulmonary pressure gradient by 55% +/- 6% and improved arterial and venous oxygen saturations by 37% +/- 29% and 11% +/- 3%, respectively. Mean systemic arterial and left atrial pressures remained nearly unchanged. No toxic side effect was observed in any patient. CONCLUSION Inhaled nitric oxide may play an important role in the management of transient critical pulmonary perfusion caused by reactive elevated pulmonary vascular resistance in the early postoperative period after Fontan-type operations and bidirectional Glenn anastomosis.

Activation of the clotting system during extracorporeal membrane oxygenation in term newborn infants

OBJECTIVES To determine the degree of clotting activation that occurs with the usual anticoagulation regimen with systemic heparinization. METHODS To allow a standardized comparison of the patients, this study focused on the first 48 hours of extracorporeal membrane oxygenation (ECMO) in term newborn infants. The ECMO perfusion circuit consisted of a roller pump, silicone membrane lungs, and silicone rubber tubing. Coagulation was controlled routinely by measuring prothrombin time, fibrinogen, antithrombin III, and reptilase time. Platelet counts, activated clotting time, and heparin concentration were controlled regularly. The following specific activation markers of the clotting system were measured: prothrombin activation fragment 1 + 2(F1+2), thrombin-antithrombin III complexes, and D-dimer. Measurements were done before the start of ECMO, after 5 minutes, and at hours 1, 2, 3, 4, 6, 12, 24 and 48. RESULTS All seven term infants had excessively high levels of clotting activation markers within the first 2 hours of ECMO: F1+2, 11.6(+/- O.9) nmol/L (mean +/- SEM); thrombin-antithrombin, 920(+/- 2.2) microg/L; D-dimer, 15.522(+/- 3.689) ng/L. During the next 46 hours of ECMO, F1+2 and thrombin-antithrombin III complexes decreased from those high values, whereas D-dimer did not. The increase of activation markers was accompanied by low fibrinogen, low platelet counts. and prolongation of reptilase time. CONCLUSIONS These findings fit the pattern of consumptive coagulopathy during neonatal ECMO, especially in the first 24 hours.

Inhaled Nitric Oxide versus Inhaled Prostacyclin and Intravenous versus Inhaled Prostacyclin in Acute Respiratory Failure with Pulmonary Hypertension in Piglets

ABSTRACT: This study was a prospective, randomized design to compare oxygenation and pulmonary hemodynamics between inhaled nitric oxide (NO) and inhaled prostacylcin (PGI2), and between inhaled and i.v. PGI2 in acute respiratory failure with pulmonary hypertension. Acute respiratory failure with pulmonary hypertension was induced in 12 piglets weighing 9–12 kg by repeated lung lavages and a continuous infusion of the stable endoperoxane analogue of thromboxane. Thereafter the animals were randomly assigned either for NO or PGI2 application. All animals were treated with different concentrations of NO or different doses of PGI2 applied i.v. and inhaled in random order. Continuous monitoring included ECG, central venous pressure (CVP), mean pulmonary artery pressure (MPAP), mean arterial pressure (MAP), artertial oxygen saturation (SaO2), and mixed venous oxygen saturation (SvO2) measurements. NO inhalation of 10 ppm resulted in a significant increase in Pao2/fraction of inspired oxygen (FiO2) from 7.8 ± 1.34 kPa to 46.1 ± 9.7 kPa. MPAP decreased significantly from 5.1 ± 0.26 kPa to 3.7 ± 0.26 kPa during inhaled NO of 40 ppm; i.v. infusion of PGI2 slightly increased oxygenation parameters. A significant increase in Pao2/FiO2 up to 32.4 ± 3.1kPa was observed during PGI2 aerosol delivery (p < 0.01); i.v. PGI2 decreased MAP from 11.5 ± 0.39 kPa to 9.8 ± 0.66 kPa (p < 0.05) and MPAP from 5.8 ± 0.53 kPa to 4.5 ± 0.66 kPa, respectively (p < 0.05). PGI2 aerosol delivery significantly decreased the MPAP to 3.7 ± 0.53 kPa (p < 0.05) without influencing the MAP. It was concluded that inhaled NO and inhaled PGI2 act as selective pulmonary vasodilators in acute respiratory failure with pulmonary hypertension resulting in improved oxygenation mainly due to improved mismatch of pulmonary perfusion and ventilation. Intravenous PGI2 improves oxygenation and pulmonary hemodynamics to a lesser extent than aerosolized PGI2 and has the risk of systemic hypotension at a higher dose.

Late dissection of the ascending aorta after previous cardiac surgery: risk, presentation and outcome.

OBJECTIVE Aortic dissection is a potentially life-threatening condition and may follow surgical interventions as a complication with distinct presentation and high mortality. Information on the incidence and etiology of aortic dissections following cardiac surgery is sparse and inconsistent. The true incidence of this entity may so far have been underestimated. METHODS Data of 223 operations on the thoracic aorta performed exclusively at our institution between January 1990 and May 2001 were analysed for clinical and prognostic features. Patients with Marfan syndrome and traumatic cases were not included. Cases of type A aortic dissection following cardiac surgery were investigated further. RESULTS Dissection of the ascending aorta occurred in 83 patients, of whom 11 (13.2%, six acute and five chronic) had undergone previous cardiac surgery (four aortic valve replacements (AVR), two double valve replacements (DVR), two AVR+coronary artery bypass grafts (CABG), three CABGs). The time interval between first operation and dissection was 0.2-17 years (median 3.3 years). Eight (72%) patients had arterial hypertension. The aortic diameter was >or=50mm in all 11 cases upon presentation. Dissections were treated with Bentall procedures (3), Cabrol procedure (1), supracoronary tube graft (6) including concomitant CABG (3) and AVR with local repair (1). Total in-hospital mortality was 54% (6/11), and 66% (4/6) in cases with acute dissection due to low cardiac output (3) and myocardial infarction (3). CONCLUSIONS Type-A aortic dissection can follow cardiac operations at any time with no typical interval or associated histology and with high overall hospital mortality. Male patients with arterial hypertension are at increased risk. Clinical presentation may differ from primary dissection with implications for management and risk estimation.

Nitric oxide 2

Introduction: Permissive hypercapnia (PH) is a beneficial strategy for patients with acute respiratory distress syndrome (ARDS) to minimize barotrauma by decreasing the peak inspiratory pressure (PIP). Hypercapnia and hypoxia cause pulmonary vasoconstriction, pulmonary artery (PA) hypertension, and, thus, an increased afterload to the right ventricle. This increased afterload may result in increased right ventricular (RV) work load and subsequent RV dysfunction. One therapeutic approach is the use of inhaled nitric oxide (iNO), a selective PA vasodilator. The objectives of this study were to test the hypothesis that in a swine model of ARDS with PH, iNO would improve RV work load and not change intrinsic RV contractility. Methods: In 11 swine (25-35 kg), ARDS was induced by surfactant depletion. Hypercapnia was achieved by decreasing the PIP while increasing the PEEP to maintain a constant mean airway pressure. iNO was administered in concentrations of 2, 5, and 10 ppm in a random order, Pulmonary blood flow (Qpa) was determined by an ultrasonic flow probe. RV total power (TP) and stroke work (SW) were calculated by Fourier transformation of the PA pressure (Ppa) and Qpa data. Preload recruitable stroke work (PRSW), a preload and afterload independent measure of ventricular contractility, was determined by a shell-subtraction method and vena caval occlusion) Results: Data are represented as mean ± sent and compared by two-way analysis of variance with repeated measures. (* n < 0.05 vs. 0 nnm) 0 ppm 2 ppm 5 ppm 10 ppm er s*1000 /mL 24.6 ± 1.6 25.2 ± 2.4 23.3 ± 1.8 22.9 ± 2.5 mW 92±11 74±6* 66±6 75±8* [RSW

Partial liquid ventilation combined with inhaled nitric oxide in acute respiratory failure with pulmonary hypertension in piglets

This study was a prospective, randomized, controlled design to evaluate gas exchange, lung mechanics, and pulmonary hemodynamics during partial liquid ventilation (PLV) combined with inhaled nitric oxide (NO) in acute respiratory failure (ARF) with pulmonary hypertension (PH). ARF with PH was induced in 12 piglets weighing 9.7-13.7 kg by repeated lung lavages and the continuous infusion of the stable endoperoxane analog of thromboxane. Thereafter the animals were randomly assigned either for PLV or conventional mechanical ventilation (CMV) at a fractional concentration of inspired O2(Fio2) of 1.0. Perfluorocarbon (PFC) liquid (30 mL kg-1) was instilled into the endotracheal tube over 5 min followed by 5 mL kg-1h-1. All animals were treated with different concentrations of NO (1-10-20 ppm) inhaled in random order. Continuous monitoring included ECG, right atrial (Pra), mean pulmonary artery (Ppa), pulmonary capillary(Ppc′), and mean arterial (Pa) pressures, arterial oxygen saturation, and mixed venous oxygen saturation measurements. During PLV Pao2/Fio2 increased significantly from 8.2 ± 0.4 kPa to 34.8 ± 5.1kPa (p < 0.01), whereas Pao2/FiO2 remained constant at 9.5 ± 0.4 kPa during CMV. The infusion of the endoperoxane analog resulted in a sudden decrease of Pao2/Fio2 from 34.8 ± 5.1 kPa to 14.1 ± 0.4 kPa (p < 0.01) in the PLV group and from 9.5 ± 0.4 kPa to 6.9 ± 0.2 kPa(p < 0.05) in the control group. Inhaled NO significantly improved oxygenation in both groups (Pao2/Fio2: 45.7 ± 5.3 kPa during PLV and 25.9 ± 4.7 kPa during CMV). During inhalation of NO mean Ppa decreased significantly from 7.8 ± 0.26 kPa to 4.2 ± 0.26 kPa (p < 0.01) in the PLV group and from 7.4 ± 0.26 kPa to 5.1 ± 0.13 kPa (p < 0.01) in the control group. As documented in the literature PLV significantly improves oxygenation and lung mechanics in severe ARF. In addition, when ARF is associated with severe PH, the combined treatment of PLV and inhaled NO improves pulmonary hemodynamics resulting in better oxygenation.

Venous thrombosis in and after extracorporeal membrane oxygenation: detection and follow-up by color Doppler sonography

The purpose of our study was to evaluate thrombosis of venous vessels during and after extracorporeal membrane oxygenation (ECMO) using color Doppler sonography. We prospectively performed serial color Doppler sonography investigations in 30 ECMO patients [age: newborn to 3 years, male:female = 20:10, venoarterial (VA) ECMO = 18, venovenous (VV) ECMO = 12]. During ECMO obstruction and/or thrombosis of the superior vena cava (SVC) was observed in 2 neonates on VA ECMO. Furthermore, a thrombotic clot from an initially open duct of Arantii with partial portal vein thrombosis, reaching into the inferior vena cava (IVC), occurred despite adequate heparinization. After ECMO, late septic SVC thrombus occurred in one neonate. IVC thrombus was observed in two pediatric VV ECMO patients. The overall incidence of venous clots was 20 % (6 of 30). Routine color Doppler sonography monitoring of vessels in children on and after ECMO was found to be useful for early detection of venous thrombosis. It enabled consequent administration of appropriate therapy as well as follow-up after decannulation and reconstruction.

The effect of positive end-expiratory pressure during partial liquid ventilation in acute lung injury in piglets.

OBJECTIVES To investigate the effects of positive end-expiratory pressure (PEEP) application during partial liquid ventilation (PLV) on gas exchange, lung mechanics, and hemodynamics in acute lung injury. DESIGN Prospective, randomized, experimental study. SETTING University research laboratory. SUBJECTS Six piglets weighing 7 to 12 kg. INTERVENTIONS After induction of anesthesia, tracheostomy, and controlled mechanical ventilation, animals were instrumented with two central venous catheters, a pulmonary artery catheter and two arterial catheters, and an ultrasonic flow probe around the pulmonary artery. Acute lung injury was induced by the infusion of oleic acid (0.08 mL/kg) and repeated lung lavage procedures with 0.9% sodium chloride (20 mL/kg). The protocol consisted of four different PEEP levels (0, 5, 10, and 15 cm H2O) randomly applied during PLV. The oxygenated and warmed perfluorocarbon liquid (30 mL/kg) was instilled into the trachea over 5 mins without changing the ventilator settings. MEASUREMENTS AND MAIN RESULTS Airway pressures, tidal volumes, dynamic and static pulmonary compliance, mean and expiratory airway resistances, and arterial blood gases were measured. In addition, dynamic pressure/volume loops were recorded. Hemodynamic monitoring included right atrial, mean pulmonary artery, pulmonary capillary wedge, and mean systemic arterial pressures and continuous flow recording at the pulmonary artery. The infusion of oleic acid combined with two to five lung lavage procedures induced a significant reduction in PaO2/FI(O2) from 485 +/- 28 torr (64 +/- 3.6 kPa) to 68 +/- 3.2 torr (9.0 +/- 0.4 kPa) (p < .01) and in static pulmonary compliance from 1.3 +/- 0.06 to 0.67 +/- 0.04 mL/cm H2O/kg (p < .01). During PLV, PaO2/FI(O2) increased significantly from 68 +/- 3.2 torr (8.9 +/- 0.4 kPa) to >200 torr (>26 kPa) (p < .01). The highest PaO2 values were observed during PLV with PEEP of 15 cm H2O. Deadspace ventilation was lower during PLV when PEEP levels of 10 to 15 cm H2O were applied. There were no differences in hemodynamic data during PLV with PEEP levels up to 10 cm H2O. However, PEEP levels of 15 cm H2O resulted in a significant decrease in cardiac output. Dynamic pressure/volume loops showed early inspiratory pressure spikes during PLV with PEEP levels of 0 and 5 cm H2O. CONCLUSIONS Partial liquid ventilation is a useful technique to improve oxygenation in severe acute lung injury. The application of PEEP during PLV further improves oxygenation and lung mechanics. PEEP levels of 10 cm H2O seem to be optimal to improve oxygenation and lung mechanics.

Hemodynamic effects of different modes of mechanical ventilation in acute cardiac and pulmonary failure: an experimental study.

Objective: To determine the hemodynamic effects of four different modes of mechanical ventilation in an animal model of acute cardiac and pulmonary failure. Design: Prospective, randomized, crossover design. Setting: University research laboratory. Subjects: Twelve piglets weighing 10 to 16 kg. Interventions: The experimental protocol consisted of three stable 30‐min periods: when ventricular and pulmonary functions were normal (control), after the induction of acute cardiac failure by the administration of a &bgr;‐adrenergic receptor blocker, and after pulmonary failure induced by repeated lung lavage. Modes of mechanical ventilation included controlled mechanical ventilation, high‐frequency oscillation, synchronized high‐frequency jet ventilation, and external negative pressure oscillation combined with pressure support ventilation. Each mode of respiratory support was randomly and sequentially applied to each animal with the assessment of cardiopulmonary function at the end of each period. Measurements and Main Results: Continuous monitoring included electrocardiogram, right atrial, left ventricular end‐diastolic, pulmonary arterial, intrathoracic aortic, arterial, esophageal, and transpulmonary pressures and arterial and mixed venous oxygen saturation measurements. In addition, cardiac output using the thermodilution technique was measured intermittently. Whereas in the control period cardiac index was significantly ( p < .05) higher during synchronized high‐frequency jet ventilation (193 ± 19.3 mL/kg/min) than during controlled mechanical ventilation (151 ± 12.1 mL/kg/min) and high‐frequency oscillation (151 ± 18.1 mL/kg/min), there was no significant hemodynamic difference between the four modes of mechanical ventilation in the cardiac and pulmonary failure periods. In the pulmonary failure period, transpulmonary pressure was significantly higher during high‐frequency oscillation (7.1 ± 1.6 mm Hg) than during controlled mechanical ventilation (5.6 ± 0.6 mm Hg), high‐frequency ventilation (4.1 ± 0.4 mm Hg), and external negative pressure oscillation combined with pressure support ventilation (5.3 ± 0.5 mm Hg). Conclusions: Synchronized high‐frequency ventilation improves cardiac performance in control conditions. No hemodynamic difference is present between the four modes of mechanical ventilation in the cardiac and pulmonary failure periods. External negative pressure oscillation combined with pressure support ventilation has moderate hemodynamic advantages over controlled mechanical ventilation and high‐frequency oscillation in different clinical settings, but it also results in a deterioration of pulmonary gas exchange during the pulmonary failure period. (Crit Care Med 1994; 22:1624–1630)