Supplemental inhaled gases alter tidal volume delivery and measurement.

OBJECTIVE: Supplemental inspired nitrogen (N(2)) or carbon dioxide (CO(2)) is commonly used to balance pulmonary blood flow in patients with single-ventricle physiology. The objective of this study was to assess if supplemental inspired gas alters delivery or measurement of tidal volume (V(T)) by a ventilator. DESIGN: Prospective, experimental study. SETTING: Respiratory Care Laboratory, Cincinnati Children's Hospital. INTERVENTIONS: Using a test lung, expired V(T) measurements from Servo 300 ventilators were compared with actual delivered V(T) (true V(T)) at baseline and during supplemental N(2) or CO(2) administration to mimic clinical use in single-ventricle patients. At compliance settings simulating normal and compromised lung function, true V(T) was determined by the test lung and inline Pneumotach. True and measured V(T) were compared by repeated-measures analysis of variance with significance defined as p < .05. MEASUREMENTS AND MAIN RESULTS: With normal lung compliance, supplemental gas administration increases both true and measured V(T), and expired V(T) measurements remain accurate. With poor lung compliance, supplemental gas flow disproportionately affects V(T) measurement. Poor lung compliance reduces true V(T) markedly (p < .001), causing a large discrepancy between true and measured V(T). Supplemental gas administration amplifies this discrepancy because the additional gas flow in the circuit erroneously augments expired V(T) measurements by the ventilator (p < .001). The discrepancy is greatest with higher-set V(T) and greater supplemental gas flow. CONCLUSIONS: The addition of supplemental inspired gas directly into the ventilator circuit can alter tidal volume delivery or measurement by a ventilator. The extent and magnitude of the alterations are determined by lung compliance. Variable effects of supplemental gas administration may confound ventilator management of patients with single-ventricle physiology.

Inhaled nitric oxide increases endothelin-1 levels: a potential cause of rebound pulmonary hypertension.

OBJECTIVE: Inhaled nitric oxide (iNO) is front-line therapy for pulmonary hypertension after repair of congenital heart disease. However, little clinical data exists regarding the effects of iNO on regulators of pulmonary vascular resistance. An imbalance between primary vasodilators, such as NO, and vasoconstrictors, such as endothelin-1 (ET-1), has been implicated in rebound pulmonary hypertension upon iNO withdrawal. The objective of this study was to determine whether iNO therapy alters plasma ET-1 levels. DESIGN: This is a prospective study involving pediatric and adult patients at risk for pulmonary hypertension. SETTING: Pediatric patients were in the cardiac intensive care unit and adult patients were in a tertiary-care hospital. PATIENTS: Group 1 included children with congenital heart disease requiring iNO for treatment of pulmonary hypertension after cardiopulmonary bypass (n = 15), group 2 was adults receiving iNO (n = 10), and group 3 included children at risk for pulmonary hypertension after bypass that did not require iNO (n = 8). INTERVENTIONS: Dosages of iNO were 2-60 ppm. The duration of therapy ranged from 23 to 188 hrs in group 1 and 29 to 108 hrs in group 2. MEASUREMENTS AND MAIN RESULTS: Arterial blood was obtained for the measurement of ET-1 levels before and during iNO therapy and 24 hrs after iNO withdrawal. Group 1 mean ET-1 levels increased to 127% of baseline by 12 hrs of iNO, remained elevated at 48 hrs (p < .05), then decreased to 71% of iNO levels 24 hrs after withdrawal (p < .01). Group 2 ET-1 levels increased to 147%, and 137% of baseline at 12 and 24 hrs of iNO therapy, then fell to 68% of baseline within 24 hrs of discontinuing iNO. ET-1 levels in group 3 decreased after surgery (p < .05). CONCLUSIONS: These data suggest that iNO increased plasma ET-1 levels, which subsequently decreased when iNO was discontinued. Increased circulating ET-1 levels might contribute to rebound pulmonary hypertension upon iNO withdrawal.