Effect of age and chronic obstructive pulmonary disease on the Breathalyzer estimation of blood alcohol level.

Twenty volunteers, 10 with chronic obstructive pulmonary disease (COPD) and 10 with no disease, ingested a vodka cocktail. Serial determinations of blood alcohol level (BAL) by gas-liquid chromatography and simultaneous Breathalyzer estimations of BAL were used to calculate blood:breath alcohol partition coefficients (PCs). Data from the present study were combined with data obtained in a previous study using identical methodology to examine the relationship between age and BAL estimation. It was found that the Breathalyzer significantly underestimated BAL as a function of age. It was hypothesized that the underestimation may be due to closing volume (CV) as the Breathalyzer samples end-expiratory breath.

Treatment of canine permeability pulmonary edema: short-term effects of dobutamine, furosemide, and hydralazine.

The effects of treatment of oleic acid pulmonary edema with dobutamine, furosemide, and hydralazine on cardiopulmonary function in 24 dogs were investigated. Pulmonary capillary wedge pressure (PCWP) was adjusted to approximately 7 mm Hg; 45 min after oleic acid (0.08 ml/kg), dogs were randomly divided into a control group, in which PCWP was maintained at approximately 7 mm Hg, and into treatment groups as described above. Mean time-averaged PCWP was 2.3 mm Hg in dogs treated with dobutamine, 4.1 mm Hg with furosemide, and 4.4 mm Hg with hydralazine. Four hours of treatment with dobutamine and furosemide significantly (p less than .01) reduced accumulation of lung water compared with the control and hydralazine groups. Qs/Qt was lower (p less than .05) with dobutamine and furosemide compared with the other groups. In dogs given hydralazine, cardiac output (CO) and systemic vascular resistance (SVR) remained constant over the 4 hr treatment interval. In contrast, in all other groups, SVR increased and CO decreased (both p less than .05). The short-term pulmonary effects of the above drugs are probably explained by differences in PCWP and/or by regional pulmonary vascular effects.

Treatment of shock in a canine model of pulmonary embolism.

Despite the high mortality (greater than 30%) associated with hypotension complicating pulmonary embolism, previous studies have not systematically investigated how best to treat shock resulting from pulmonary embolism. In 24 dogs, we measured relevant hemodynamic parameters before and after shock was produced by intravenously injected autologous blood clots. When systemic blood pressure fell to 70 mmHg, dogs were randomly divided into groups and treated blindly for 1 h. All control dogs and all dogs treated with volume and isoproterenol died. In contrast, all dogs treated with noradrenaline were resuscitated and remained hemodynamically stable for 1 h. This effect of noradrenaline was significant (p less than 0.01, Fisher's exact test). Noradrenaline improved right ventricular performance by increasing blood pressure and improving right ventricular perfusion and/or by a direct increase in contractility. We conclude that in a canine model of pulmonary embolism and shock, noradrenaline may be the drug of choice for acute resuscitation.

Effects of dopamine on cardiopulmonary function and left ventricular volumes in patients with acute respiratory failure.

We investigated cardiopulmonary effects of dopamine in patients with acute respiratory failure. Specifically, we wished to test the hypothesis that left ventricular filling pressure (Pcwp) would increase when cardiac output (CO) increased with dopamine. Dopamine (range, 5.5 to 20 micrograms/kg/min) increased blood pressure (BP) (p less than 0.001) Pcwp, CO, and stroke volume (SV) (p less than 0.005). Mean Pcwp increased (p less than 0.005) 45% with dopamine, from 11 to 16 mmHg. Qs/Qt increased with dopamine in association with an increase in mixed venous O2 tension, and arterial O2 tension remained constant. In 8 of these patients, left ventricular end-diastolic volume (LVEDV) and end-systolic volume (ESV) were measured using scintigraphic techniques. The LVEDV increased (p less than 0.01) in each patient after the administration of dopamine, and the mean change was from 134 to 163 ml. Although BP and LV afterload increased in each patient, there was no consistent change in LVESV after dopamine administration, i.e., ESV decreased in 1 patient, remained constant in 3, and increased in 4. Accordingly, because afterload increased in all patients and ESV did not, dopamine probably increased contractility. Because EDV increased in all patients, we concluded that the increase in SV with dopamine is explained by a combination of inotropic and peripheral vascular effects.