Supraarterial decompression myotomy for myocardial bridging in a child.

A 10-year-old boy presented with a history of exertional chest pain. An electrocardiogram demonstrated an inferior apical myocardial infarction. Cardiac catheterization revealed myocardial bridging of the left anterior descending coronary artery with evidence of intramyocardial obstruction during systole. The patient underwent successful treatment with supraarterial decompression myotomy and remains symptom free at 1 year.

Method for creation of the aortotomy site for saphenous vein grafts.

Saphenous vein coronary artery bypass grafting requires a proximal anastomosis of the vein to the aorta. A variety of techniques have been described to create the aortotomy. We have developed a four-sided knife (Xcision Scalpel; patent pending, Research Medical, Inc, Midvale, UT) that facilitates the creation of a more uniform circular aortotomy. The purpose of this communication is to describe the knife and the technique for its use.

Inhaled nitric oxide, right ventricular efficiency, and pulmonary vascular mechanics: selective vasodilation of small pulmonary vessels during hypoxic pulmonary vasoconstriction.

OBJECTIVE: In the setting of acute pulmonary artery hypertension, techniques to reduce right ventricular energy requirements may ameliorate cardiac failure and reduce morbidity and mortality. Inhaled nitric oxide, a selective pulmonary vasodilator, may be effective in the treatment of pulmonary artery hypertension, but its effects on cardiopulmonary interactions are poorly understood. METHODS: We therefore developed a model of hypoxic pulmonary vasoconstriction that mimics the clinical syndrome of acute pulmonary hypertension. Inhaled nitric oxide was administered in concentrations of 20, 40, and 80 ppm. RESULTS: During hypoxic pulmonary vasoconstriction, the administration of nitric oxide resulted in a significant improvement in pulmonary vascular mechanics and a reduction in right ventricular afterload. These improvements were a result of selective vasodilation of small pulmonary vessels and more efficient blood flow through the pulmonary vascular bed (improved transpulmonary vascular efficiency). The right ventricular total power output diminished during the inhalation of nitric oxide, indicating a reduction in right ventricular energy requirements. The net result of nitric oxide administration was an increase in right ventricular efficiency. CONCLUSION: These data suggest that nitric oxide may be beneficial to the failing right ventricle by improving pulmonary vascular mechanics and right ventricular efficiency.

Contrast echocardiography: influence of ultrasonic machine settings, mixing conditions, and pressurization on pixel intensity and microsphere size of Albunex solutions in vitro.

To use Albunex as a blood-flow tracer, the stability and consistency of microspheres under mixing conditions must be known. This study examined the effects of mixing conditions and machine settings on the size and echogenicity of Albunex solutions in vitro. Acoustic power, log compression, time-gain compensation, and transducer frequency were varied as Albunex solutions were imaged after mixing with magnetic stirring and pressurized. Higher acoustic power and lower transducer frequency decreased mean pixel intensity of Albunex solution images over time. Intensity, size, and number of Albunex microspheres were not significantly different between stirring speeds. The echogenicity of the Albunex solutions decreased with pressurization, and the critical pressure necessary to reduce the intensity to half its initial value increased with the logarithm of concentration (r = 0.91; p < 0.001). The microsphere size decreased with pressurization and remained smaller after pressure release (3.66 +/- 2.13 versus 1.47 +/- 0.95 microns; p < 0.01). These data indicate that acoustic power and transducer frequency may affect the physical properties of Albunex microspheres, decreasing mean videointensity. Pressure sensitivity of Albunex caused the decrease of videointensity and microsphere size.

Nitric oxide improves transpulmonary vascular mechanics but does not change intrinsic right ventricular contractility in an acute respiratory distress syndrome model with permissive hypercapnia.

OBJECTIVE: To test the hypothesis that in a swine model of acute respiratory distress syndrome (ARDS) with permissive hypercapnia, inhaled nitric oxide would improve transpulmonary vascular mechanics and right ventricular workload while not changing intrinsic right ventricular contractility. DESIGN: Prospective, randomized, controlled laboratory trial. SETTING: University research laboratory. SUBJECTS: Eleven swine (30 to 46 kg). INTERVENTIONS: The swine were anesthetized, intubated, and paralyzed. After median sternotomy, pressure transducers were placed in the right ventricle, pulmonary artery, and left atrium. An ultrasonic flow probe was placed around the pulmonary artery. Ultrasonic dimension transducers were sutured onto the heart at the base, apex, left ventricle (anterior, posterior, free wall), and right ventricle (free wall). An additional transducer was placed in the interventricular septum. A surfactant depletion model of ARDS was created by saline lung lavage. Nitric oxide was administered at 2, 4, and 6 parts per million (ppm), in a random order, under the condition of permissive hypercapnia (Paco2 55 to 75 torr [7.3 to 10.0 kPa]). MEASUREMENTS AND MAIN RESULTS: We evaluated the pulmonary vascular and right ventricular effects of permissive hypercapnia, with and without inhaled nitric oxide, by measuring variables of transpulmonary vascular mechanics and right ventricular function. These variables included mean pulmonary arterial pressure, right ventricular total power, right ventricular stroke work, transpulmonary vascular efficiency, and right ventricular intrinsic contractility. Data were obtained after lung injury under the following conditions: a) normocapnia (Paco2 35 to 45 torr [4.7 to 6.0 kPa]) and nitric oxide at 0 ppm; b) hypercapnia and nitric oxide at 0 ppm; c) hypercapnia and nitric oxide at 2, 4, and 6 ppm; and d) repeat measurements with hypercapnia and nitric oxide at 0 ppm. In ARDS with permissive hypercapnia, inhaled nitric oxide therapy (2 to 6 ppm) improved transpulmonary vascular mechanics and right ventricular workload by lowering pulmonary arterial pressure (29.6 +/- 1.3 vs. 24.6 +/- 1.0 mm Hg, p = .0001), increasing transpulmonary vascular efficiency (13.9 +/- 0.5 vs. 16.1 +/- 0.7 L/W-min, p = .0001), decreasing right ventricular total power (142 +/- 9 vs. 115 +/- 9 mW, p = .001), and decreasing right ventricular stroke work (653 +/- 37 vs. 525 +/- 32 ergs x 10(3), p = .001). Inhaled nitric oxide did not change right ventricular contractility, as measured by preload-recruitable stroke work. CONCLUSIONS: Inhaled nitric oxide ameliorated any negative effects of hypoxic and hypercapnic pulmonary vasoconstriction. The beneficial effects of inhaled nitric oxide are related to alterations in right ventricular afterload and not intrinsic right ventricular contractility. The improved cardiopulmonary effects of inhaled nitric oxide with permissive hypercapnia potentially expand the use of nitric oxide in ARDS and other conditions in which this strategy is employed.

In acute lung injury, inhaled nitric oxide improves ventilation-perfusion matching, pulmonary vascular mechanics, and transpulmonary vascular efficiency.

Acute respiratory distress syndrome continues to be associated with significant morbidity and mortality related to ventilation-perfusion mismatch, pulmonary hypertension, and right ventricular failure. It has been suggested that inhaled nitric oxide, which is a selective pulmonary vasodilator, may be effective in the treatment of acute respiratory distress syndrome; however, the effects of nitric oxide on cardiopulmonary interactions are poorly understood. We therefore developed a model of acute lung injury that mimics the clinical syndrome of acute respiratory distress syndrome. In our model, inhaled nitric oxide significantly reduced pulmonary artery pressure, pulmonary vascular resistance, and pulmonary vascular impedance. In addition, inhaled nitric oxide improved transpulmonary vascular efficiency and ventilation-perfusion matching, which resulted in increased arterial oxygen tension. Although arterial oxygen tension increased, oxygen delivery did not improve significantly. These data suggest that by improving ventilation-perfusion matching and arterial oxygen tension while lowering pulmonary vascular resistance and impedance, nitric oxide may be beneficial in patients with acute respiratory distress syndrome. However, additional measures to enhance cardiac performance may be required.