Monitoring Exhaled Carbon Dioxide.

In the past few decades, assessment of exhaled CO2 in both intubated and non-intubated patients has evolved into an essential component in many aspects of patient monitoring. Besides the basic assessment of ventilation, exhaled CO2 monitoring can provide valuable patient safety information and critical physiologic data in regard to the ventilation and perfusion matching in the lungs, cardiac output, and metabolic rate. Despite these important clinical monitoring benefits and widespread availability, exhaled CO2 monitoring is often underutilized. The purpose of this paper is to review the importance and present the extensive body of knowledge to support the use of exhaled CO2 monitoring in various areas of clinical practice. Advanced application concepts and the future development of exhaled CO2 monitoring will also be discussed.

Calculation of physiologic dead space: comparison of ventilator volumetric capnography to measurements by metabolic analyzer and volumetric CO2 monitor.

BACKGROUND: Calculation of physiologic dead space (dead space divided by tidal volume [VD/VT]) using the Enghoff modification of the Bohr equation requires measurement of the partial pressure of mean expired CO2 (PECO2) by exhaled gas collection and analysis, use of a metabolic analyzer, or use of a volumetric CO2 monitor. The Dräger XL ventilator is equipped with integrated volumetric CO2 monitoring and calculates minute CO2 production (VCO2). We calculated PECO2 and VD/VT from ventilator derived volumetric CO2 measurements of VCO2 and compared them to metabolic analyzer and volumetric CO2 monitor measurements. METHODS: A total of 67 measurements in 36 subjects recovering from acute lung injury or ARDS were compared. Thirty-one ventilator derived measurements were compared to measurements using 3 different metabolic analyzers, and 36 ventilator derived measurements were compared to measurements from a volumetric CO2 monitor. RESULTS: There was a strong agreement between ventilator derived measurements and metabolic analyzer or volumetric CO2 monitor measurements of PECO2 and VD/VT. The correlations, bias, and precision between the ventilator and metabolic analyzer measurements for PECO2 were r = 0.97, r(2) = 0.93 (P < .001), bias -1.04 mm Hg, and precision ± 1.47 mm Hg. For VD/VT the correlations were r = 0.95 and r(2) = 0.91 (P < .001), and the bias and precision were 0.02 ± 0.04. The correlations between the ventilator and the volumetric CO2 monitor for PECO2 were r = 0.96 and r(2) = 0.92 (P < .001), and the bias and precision were -0.19 ± 1.58 mm Hg. The correlations between the ventilator and the volumetric CO2 monitor for VD/VT were r = 0.97 and r(2) = 0.95 (P < .001), and the bias and precision were 0.01 ± 0.03. CONCLUSIONS: PECO2, and therefore VD/VT, can be accurately calculated directly from the Dräger XL ventilator volumetric capnography measurements without use of a metabolic analyzer or volumetric CO2 monitor.

Are inhaled vasodilators useful in acute lung injury and acute respiratory distress syndrome?

In patients with acute respiratory distress syndrome (ARDS), inhaled vasodilator can result in important physiologic benefits (eg, improved hypoxemia, lower pulmonary arterial pressure, and improved right-ventricular function and cardiac output) without systemic hemodynamic effects. Inhaled nitric oxide (INO) and aerosolized prostacyclins are currently the most frequently used inhaled vasodilators. Inhaled prostacyclins are as effective physiologically as INO and cost less. Randomized controlled trials of INO in the treatment of ARDS have shown short-term physiologic benefits, but no benefit in long-term outcomes. No outcome studies have been reported on the use of prostacyclin in patients with ARDS. There is no role for the routine use of inhaled vasodilators in patients with ARDS. Inhaled vasodilator as a rescue therapy for severe refractory hypoxemia in patients with ARDS may be reasonable, but is controversial.

Are specialized endotracheal tubes and heat-and-moisture exchangers cost-effective in preventing ventilator associated pneumonia?

Ventilator-associated pneumonia (VAP) is a common and serious complication of mechanical ventilation via an artificial airway. As with all nosocomial infections, VAP increases costs, morbidity, and mortality in the intensive care unit (ICU). VAP prevention is a multifaceted priority of the intensive care team, and can include the use of specialized artificial airways and heat-and-moisture exchangers (HME). Substantial evidence supports the use of endotracheal tubes (ETTs) that allow subglottic suctioning; silver-coated and antiseptic-impregnated ETTs; ETTs with thin-walled polyurethane cuffs; and HMEs, but these devices also can have adverse effects. Controversy still exists regarding the evidence, cost-effectiveness, and disadvantages and risks of these devices.

Pulmonary vasodilators.

Pulmonary vasodilators are an important treatment for pulmonary arterial hypertension. They reduce pulmonary artery pressure; improve hemodynamic function; alter ventilation/perfusion matching in the lungs; and improve functional quality of life, exercise tolerance, and survival in patients with severe pulmonary arterial hypertension. This paper reviews the currently available pulmonary vasodilators and those under development, many of which can be administered via inhalation. I will also give an overview of the clinical pharmacology of, the indications for, and the evidence supporting pulmonary vasodilators, their delivery via inhalation, and potential toxic and adverse effects.

Use of dexmedetomidine to facilitate extubation in surgical intensive-care-unit patients who failed previous weaning attempts following prolonged mechanical ventilation: a pilot study.

INTRODUCTION: Dexmedetomidine is a selective alpha-2 adrenergic receptor agonist that exhibits sedative, analgesic, anxiolytic, and sympatholytic effects without respiratory-drive depression. We prospectively evaluated the use of dexmedetomidine to facilitate the withdrawal of mechanical ventilation and extubation in 5 trauma/surgical intensive-care-unit patients who had failed previous weaning attempts due to agitation and hyperdynamic cardiopulmonary response. METHODS: Intravenous infusion of dexmedetomidine commenced at 0.5 or 0.7 microg/kg/h without a loading dose. Background sedation and analgesia with propofol, benzodiazepines, and opiates was discontinued or reduced as tolerated. Dexmedetomidine infusion was titrated between 0.2 and 0.7 microg/kg/h to maintain a stable cardiopulmonary response and modified Ramsay Sedation Score between 2 and 4. RESULTS: Following dexmedetomidine administration, propofol infusion was weaned and discontinued in 4 patients. In the fifth patient, benzodiazepine and opiate infusions were reduced. Ventilatory support in all patients could be weaned to continuous positive airway pressure of 5 cm H2O without agitation, hemodynamic instability, or respiratory decompensation. All patients were extubated while receiving dexmedetomidine infusion (mean dose of 0.32 +/- 0.08 microg/kg/h). One patient required reintubation for upper-airway obstruction. CONCLUSION: Dexmedetomidine appears to maintain adequate sedation without hemodynamic instability or respiratory-drive depression, and thus may facilitate extubation in agitated difficult-to-wean patients; it therefore deserves further investigation toward this novel use.

Description and evaluation of a delivery system for aerosolized prostacyclin.

INTRODUCTION: Inhaled vasodilators such as nitric oxide and aerosolized prostacyclin (PGI(2)) are used to treat severe hypoxemia in acute respiratory distress syndrome. Preferential distribution of nitric oxide and PGI(2) to ventilated areas of the lung causes selective pulmonary vasodilation, improved ventilation/perfusion matching, and decreased hypoxemia. Because of the technical limitations of previously described methods, we developed a PGI(2) delivery technique that allows the aerosolized drug dose to be easily calculated, set, and adjusted. METHODS: A 50 mL solution of PGI(2) (3.0x10(4) ng/mL) and a 500 mL normal saline solution were infused by a dual-channel volumetric infusion pump into a MiniHEART jet nebulizer that has a manufacturer-specified output of 8 mL/h at a set flow of 2 L/min. By adjusting the pump infusion rate to achieve a total output of 8 mL/h, the PGI(2) concentration was altered to deliver a calculated aerosolized dose of 10-50 ng/kg/min. The effectiveness of the delivery system was retrospectively evaluated by way of the responses of 11 severely hypoxemic acute respiratory distress syndrome patients who received PGI(2) via the system we describe. The MiniHEART nebulizer output, particle size, and dose delivery were evaluated in a laboratory bench study, using a set flow of 2 L/min. RESULTS: Aerosolized PGI(2) therapy (mean dose 28 +/- 17 ng/kg/min, range 10-50 ng/kg/min) significantly increased the ratio of P(aO)(2) to fraction of inspired oxygen (P(aO)(2)/F(IO)(2)) (60 +/- 11 mm Hg vs 80 +/- 17 mm Hg, p = 0.003) and arterial oxygen saturation measured via pulse oximetry (86 +/- 8% vs 94 +/- 3%, p = 0.005) (differences evaluated with the Wilcoxon signed rank test). There was no difference in positive end-expiratory pressure, mean airway pressure, or F(IO)(2), before and after aerosolized PGI(2) (p > 0.05). Nebulizer output was 6.8 +/- 0.9 mL/h, range 6.0-7.8 mL/h. The inhaled aerosol particles had a mass median diameter of 3.1 micro m. Emitted dose was 67 +/- 13% (range 57-81%) of the calculated dose. CONCLUSION: Our system is effective in delivering aerosolized PGI(2) to the alveolar-capillary interface, as indicated by significant oxygenation improvements soon after therapy commenced. The performance of the MiniHEART nebulizer varies from the manufacturer's specifications, which may alter the delivered dose.