A comparison of pulmonary artery occlusion pressure and left ventricular end-diastolic pressure during mechanical ventilation with PEEP in patients with severe ARDS.

When positive end-expiratory pressure (PEEP) is applied to normal lungs, the pulmonary artery occlusion pressure (PAOP) may reflect alveolar pressure and not left ventricular end-diastolic pressure (LVEDP). The reliability of PAOP measurements has been questioned when PEEP levels greater than 10 cm H2O are applied. To verify whether this disparity occurs in patients with severe lung injury, the authors simultaneously measured both PAOP and LVEDP at 0, 10, and 16-20 cm H2O PEEP in 12 supine patients with severe adult respiratory distress syndrome (ARDS). In all patients, the radiographic location of the PA catheter tip was at or below the level of the posterior border of the left atrium. A close correlation was found between PAOP and LVEDP at each level of PEEP. In only six of 35 simultaneous measurements was the PAOP-LVEDP gradient 2 mmHg or more (2-3 mmHg in four, and 4 mmHg in two). In five patients, the highest PEEP level was 4-9 cm H2O greater than LVEDP; however, no gradient was measured between LVEDP and PAOP. The authors conclude that, in severe ARDS, a close correspondence between PAOP and LVEDP is maintained despite applying PEEP levels up to 20 cm H2O, suggesting that, in ARDS, surrounding pathology prevents transmitted alveolar pressure from collapsing adjacent pulmonary vessels.

Acute left ventricular dysfunction during unsuccessful weaning from mechanical ventilation.

The authors studied the hemodynamic effects of rapidly weaning from mechanical ventilation (MV) 15 patients with severe chronic obstructive pulmonary disease (COPD) and cardiovascular disease who were recovering from acute cardiopulmonary decompensation. In each patient, 10 min of spontaneous ventilation (SV) with supplemental oxygen resulted in reducing the mean esophageal pressure (X +/- SD, + 5 +/- 3 to -2 +/- 2.5 mmHg, P less than .01) and increasing cardiac index (CI) 3.2 +/- 0.9 to 4.3 +/- 1.3 1/min/M2, P less than .001), systemic blood pressure (BP 77 +/- 12 to 90 +/- 11 mmHg, P less than .001), heart rate (HR 97 +/- 12 to 112 +/- 16 beats/min, P less than .001), and, most importantly, transmural pulmonary artery occlusion pressure markedly increased (PAOPtm 8 +/- 5 to 25 +/- 13 mmHg, P less than .001), mandating a reinstitution of MV. In four patients with left ventricular (LV) catheters, the PAOP correlated with the LV end-diastolic pressure during both MV and SV. Gated blood pool imaging showed SV increased the LV end-diastolic volume index (65 +/- 24 to 83 +/- 32/M2, P less than .002) with LV ejection fraction unchanged. Patients were treated for a mean of 10 days with diuretics, resulting in a reduction of blood volume (4.55 +/- 0.9 1 to 3.56 +/- 0.55 1) and body weight (-5 kg, P less than .001). Subsequently, nine of the 15 patients were weaned successfully from mechanical ventilation with unchanged PAOP.

Right ventricular function in COPD patients during weaning from mechanical ventilation.

We studied the right ventricular function during a successful weaning period in 7 COPD patients without LV disease who had been mechanically ventilated for several days after an acute exacerbation of their disease. A Swan-Ganz ejection fraction thermodilution catheter performed measurements of right ventricular ejection fraction (RVEF) and right ventricular end-diastolic volume index (RVEDVI) before and fifteen minutes after disconnection from the ventilator at the maintenance FiO2. Although pulmonary artery pressure (PAP) rose from 25 +/- 4 to 28.5 +/- 4.5 mmHg after disconnection from the ventilator, RVEF (0.36 +/- 0.56 to 0.35 +/- 0.12) and RVEDVI (117 +/- 51 to 126 +/- 52 ml/m2) remained similar in both conditions. We concluded that right ventricular systolic function assessed with modified pulmonary artery catheter was maintained during the weaning phase in such weanable patients. This method could easily detect any fall of RVEF or diastolic RV enlargement able to impair the weaning in some patients.

Diagnosis of central venous catheter-related sepsis. Critical level of quantitative tip cultures.

The results of a simplified quantitative broth dilution quantitative tip culture (QTC) of 331 central venous catheters were compared with clinical data prospectively recorded in critically III patients to diagnose bacteremic or nonbacteremic catheter-related sepsis (CRS) (36 catheters), as opposed to contamination (42 catheters) or simple colonization from a distant septic focus (seven catheters). Thirty-five of 36 catheters associated with CRS yielded 10(3) colony-forming units per milliliter (CFU/mL) or more, and 3.8 X 10(2) Candida organisms grew from one. In contrast, 5 X 10(2) CFU/mL or less grew from 37 of 42 contaminated catheters. A QTC of 10(3) CFU/mL or more was 97.5% sensitive and 88% specific for the diagnosis of CRS. The QTC appeared especially useful for the diagnosis of CRS secondary to blood-borne seeding of catheters, or associated with coagulase-negative staphylococci.

Hemodynamic effects of urapidil in patients with pulmonary hypertension. A comparative study with hydralazine.

Vasodilator therapy for pulmonary hypertension ideally should cause a proportionately greater reduction of resistance in the pulmonary vascular bed than in the systemic circulation. This should limit the occurrence of systemic hypotension, which can complicate the use of most vasodilator drugs. Urapidil is a new vasodilator that acts by postsynaptic alpha 1-blockade while inhibiting the aortic pressure baroreceptor reflex and reducing central sympathetic tone. We investigated and compared the short-term effects of Urapidil and hydralazine in 10 patients suffering varying degrees of pulmonary hypertension. Each patient received either 0.35 mg/kg hydralazine or 0.75 mg/kg Urapidil intravenously on 2 sequential days in a randomized order. The main effect of Urapidil was to decrease the mean pulmonary artery pressure in all 10 patients from 44 +/- 4 to 37 +/- 3.5 mm Hg (p less than 0.001). After Urapidil infusion, the mean decrease of resistance in the pulmonary vascular bed (32%) exceeded that in the systemic circulation (25%). In contrast, pulmonary artery pressure remained unchanged with hydralazine, and predominant systemic vasodilation occurred: systemic vascular resistance decreased by 45%, whereas pulmonary vascular resistance decreased by 25%. Hydralazine markedly increased the cardiac index and induced tachycardia. Urapidil maintained the heart rate nearly constant and only slightly increased the cardiac index, thereby fostering the diastolic emptying of the pulmonary circulation. No significant change in arterial oxygenation occurred with either drug, although arterial oxygen partial pressure tended to increase with hydralazine. Urapidil may be a promising drug in the treatment of patients with pulmonary hypertension.