Do-not-intubate status was present among one-fifth of ICU patients who received NIV. DNI patients who were alive on day 90 experienced no decrease in HRQOL compared to baseline. The prevalences of anxiety, depression, and PTSD-related symptoms in these patients and their relatives were similar to those seen after NIV was used as part of full-code management (clinicaltrial.govNCT01449331).
To investigate endothelium-dependent and endothelium-independent nitric oxide (NO) mediated pulmonary vasodilation in patients with chronic obstructive lung disease (COLD), we examined the responses to incremental infusion rates of acetylcholine (ACh) or inhaled NO on hemodynamic and gas exchange. In 13 patients, ACh (15 mg/min) decreased pulmonary artery pressure (Ppa) from 31 +/- 1 to 28 +/- 1 mm Hg (p < 0.01) and systemic arterial pressure while increasing cardiac index from 3.7 +/- 0.4 to 4.7 +/- 0.4 L/min/m2 (p < 0.01). Inhaling 40 parts per million (ppm) NO decreased Ppa from 32 +/- 1 to 26 +/- 1 mm Hg (p < 0.001) with no associated hemodynamic change. ACh reduced PaO2 from 57 +/- 3 to 48 +/- 2 mm Hg (p < 0.01) and increased venous admixture (QVA/QT) from 35 +/- 3 to 45 +/- 3% (p < 0.01). Inhaling 40 ppm NO increased PaO2 from 57 +/- 3 to 60 +/- 3 mm Hg (p < 0.01) and decreased QVA/QT from 36 +/- 3 to 32 +/- 3% (p < 0.01). Pulmonary vascular resistance changes were similar in response to 40 ppm NO or 15 mg/min ACh. In COLD patients, ACh produces both pulmonary and systemic vasodilation but impairs arterial oxygenation whereas inhaled NO induces selective pulmonary vasodilation while improving gas exchange. The resistance to ACh in some patients could be related to pulmonary endothelial dysfunction.
To define the relationship between plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) and hemodynamic parameters in patients with chronic pulmonary artery hypertension, we measured plasma concentrations of the peptide in 15 patients during right heart catheterization. Eleven patients had chronic obstructive pulmonary disease and 4 had pulmonary vascular disease of diverse etiology. At rest, plasma concentrations of IR-ANP positively correlated with mean pulmonary artery pressure (r = 0.70, p less than 0.01) and pulmonary vascular resistance (r = 0.88, p less than 0.001), but not with right atrial pressure. Nine of these patients, all with chronic obstructive pulmonary disease, were also evaluated during exercise. Plasma concentrations of IR-ANP increased from 131 +/- 22 to 191 +/- 30 pg/ml (p less than 0.003) at maximal exercise, whereas pulmonary artery pressure increased from 29 +/- 1.5 to 56 +/- 2.5 mm Hg and right atrial pressure from 5 +/- 1 to 13 +/- 2 mm Hg. Increases of plasma IR-ANP concentrations correlated with changes in pulmonary artery pressure and right atrial pressure but not with changes in pulmonary capillary wedge pressure. These findings suggest that ANP is released in response to an increase in pulmonary artery pressure and are consistent with the hypothesis that ANP could modulate the pulmonary vascular tone in patients with pulmonary artery hypertension.
To investigate the physiological role of atrial natriuretic factor (ANF) in patients with hypoxic pulmonary hypertension secondary to chronic obstructive lung disease (COLD), we infused synthetic a-human ANF in seven such patients, and investigated the physiological correlates to circulating peptide levels in 24 patients with COLD.ANF infusion, at incremental rates of 0.01, 0.03, and 0.1 Mg/kg . min, increased basal plasma immunoreactive (ir) ANF (136±38 pg/ml) by 3-, 10-, and 26-fold, respectively, and reduced pulmonary artery pressure (from 33±3 to 25±2 mmHg, P < 0.001) and systemic arterial pressure (from 88±4 to 79±4 mmHg, P < 0.001) in a dose-related fashion. Cardiac index increased by 13.5% (P < 0.01) while heart rate was unchanged. Cardiac filling pressures decreased at 0.1 Mg/kg min ANF. Pulmonary and systemic vascular resistance fell by 37% (P < 0.001) and 19% (P < 0.001), respectively. Arterial oxygenation was impaired during ANF infusion, suggesting partial reversal of hypoxic pulmonary vasoconstriction. Plasma renin activity remained unchanged but aldosterone fell by 44% (P < 0.01).The levels of plasma irANF in 24 patients correlated directly with the degree of hemoconcentration (r = 0.67, P < 0.001), respiratory acidosis (r = -0.65, P < 0.001), and pulmonary hypertension (r = 0.52, P < 0.01). The results suggest that ANF may serve as a potent pulmonary vasodilator involved in the circulatory homeostasis of patients with COLD.
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