Association of PEEP with two different inflation volumes in ARDS patients: effects on passive lung deflation and alveolar recruitment.

OBJECTIVE: To assess the effects of the association of positive end-expiratory pressure (PEEP) with different inflation volumes (V(T)'s) on passive lung deflation and alveolar recruitment in ARDS patients. DESIGN: Clinical study using PEEP with two different V(T)'s and analyzing whether passive lung deflation and alveolar recruitment (Vrec) depend on end-inspired (EILV) or end-expired (EELV) lung volume in mechanically ventilated ARDS patients. SETTING: Medical intensive care unit in a university hospital. PATIENTS AND PARTICIPANTS: Six mechanically ventilated consecutive supine patients with ARDS. INTERVENTIONS: Time-course of thoracic volume decay during passive expiration and Vrec were investigated in six ARDS patients ventilated on PEEP with baseline V(T) (V(T),b) and 0.5V(T) (0.5V(T),b), and on zero PEEP (ZEEP) with V(T),b. Time constants of the fast (tau1) and slow (tau2) emptying compartments, as well as resistances and elastances were also determined. MEASUREMENTS AND RESULTS: (a) the biexponential model best fitted the volume decay in all instances. The fast compartment was responsible for 84+/-7 (0.5V(T),b) and 86+/-5% (V(T),b) on PEEP vs 81+/-6% (V(T),b) on ZEEP (P:ns) of the exhaled V(T), with tau1 of 0.50+/-0.13 and 0.58+/-0.17 s vs 0.35+/-0.11 s, respectively; (b) only tau1 for V(T),b on PEEP differed significantly (P < 0.02) from the one on ZEEP, suggesting a slower initial emptying; (c) for the same PEEP, Vrec was higher with a higher volume (V(T)b) than at a lesser one (0.5V(T),b), reflecting the higher V(T). CONCLUSIONS: In mechanically ventilated ARDS patients: (a) the behavior of airway resistance seems to depend on the degree of the prevailing lung distension; (b) alveolar recruitment appears to be more important when higher tidal volumes are used during mechanical ventilation on PEEP; (c) PEEP changes the mechanical properties of the respiratory system fast-emptying compartment.

Effects of ischemia and reperfusion on QT dispersion during coronary angioplasty.

The effects of ischemia and reperfusion on QT interval dispersion (QTD: QTmax-QTmin in the 12-lead ECG) were analyzed in 15 patients (12 males, 57 +/- 13 years) undergoing coronary angioplasty (PTCA). All patients had single-vessel coronary artery disease (only one > or = 85% stenosis in a major coronary artery) and normal left ventricular function. All were in sinus rhythm with normal atrioventricular and intraventricular conduction on the surface ECG. No patient was on therapy that could affect the QT interval. The ECG was recorded (all 12 leads simultaneously) at 50 mm/s speed before the first balloon inflation, at the end of the first inflation during PTCA, and at 30" and 60" during reperfusion following the first inflation. In order to avoid ischemic preconditioning, only recordings of the first inflation were used. In each tracing QTmax and QTmin were evaluated. All values were rate corrected using a simple linear equation (QT linear corrected = QT + 0.154 [1-RR]). QTD increased significantly during both ischemia and reperfusion. QTmax was not changed by ischemia and was increased by reperfusion. QTmin was reduced by ischemia and increased by reperfusion. These results indicate that both ischemia and reperfusion alter ventricular repolarization, inducing a less homogeneous ventricular recovery pattern.

Influence of age, lead axis, frequency of arrhythmic episodes, and atrial dimensions on P wave triggered SAECG in patients with lone paroxysmal atrial fibrillation.

Signal-averaged P wave of 42 patients with lone paroxysmal atrial fibrillation (PAF) and 29 normal subjects (N) were recorded, using three orthogonal leads and analyzed in the time and frequency (entire P wave or a 100-ms segment ranging from 75 ms before to 25 ms after the end of P wave) domains. PAFs were divided into a group of 12 having > or = 2 attacks a month (HF) and a group of 30 having < or = 2 attacks a year (LF). Statistically significant differences were absent with regard to ages of PAF and N; ages of HF, LF, and N at the time of signal-averaged ECG; ages of HF and LF at the time of the first arrhythmic episode; and elapsed times from the first episode. Length of P wave and some frequency-domain parameters were found to be significantly correlated with age. PAF showed a significantly longer duration of P wave in the frontal plane using the time-domain analysis. Frequency analysis was found to be useful in evaluating the influence of attack frequency. HF showed significantly higher values of some frequency-domain parameters than LF and N, while the three groups did not differ for time-domain analysis. P wave duration and frequency content of the three orthogonal leads proved to be significantly different in PAF and N. Right and left atrial echocardiographic dimensions proved to be higher (even if within normal limits) in HF than in LF and N. Results suggest that frequency analysis should be performed on the entire P wave.

Wavelength index at three atrial sites in patients with paroxysmal atrial fibrillation.

The purpose of this study was to evaluate the wavelength index (WLI) at three atrial sites in a group of 23 patients with recurrent episodes of lone paroxysmal atrial fibrillation (LPAF) and a control group (n = 20). All patients underwent programmed atrial stimulation (paced cycle length = 600 ms) at high, medium, and low lateral right atrial wall. P wave duration, sinus cycle length, and corrected sinus node recovery time were not significantly different between the two study groups. WLI was calculated according to the following formulas: atrial effective refractory period (AERP)/duration of atrial extrastimulus electrogram (A2) or AERP/A2 + atrial latency; and atrial functional refractory period (AFRP)/A2. WLI was significantly shorter in LPAF than in the control group at each of the paced atrial sites independently of the formula used. Duration of premature atrial electrogram appeared to play the major role in determining the difference in WLI between patients with paroxysmal atrial fibrillation and the control group.

Heart rate variability and functional severity of congestive heart failure secondary to coronary artery disease.

To investigate the behaviour of heart rate variability (HRV) with the advancing severity of heart failure (CHF) we studied 20 normal subjects and 80 coronary artery disease (CAD) patients in sinus rhythm. CAD patients were selected consecutively in order to form four equal groups of 20 subjects with different degrees of CHF according to the New York Heart Association (NYHA) functional classification. In each subject a 24 h ECG Holter tape was recorded and subsequently analysed to obtain measures of heart rate and HRV. We used several measures of HR and both spectral and non-spectral measures of HRV. Among these we employed the width of the R-R interval distribution over 24 h at three different heights (TV, 10%Var, 50%Var). The CAD group showed significantly lower HRV counts and smaller spectral components than controls. However, these differences were due to the presence of CHF rather than to CAD. Indeed, a progressive and significant increase in heart rate and a contemporary decrease in HRV was observed with the advancing severity of CHF. Class IV patients had the smallest HR variation; the spectral composition in this group was barely detectable. The decrease in time domain measures of HRV followed the increase in NYHA Class in a progressive and regular pattern, while the low frequency and high frequency spectral power showed the largest reduction from NYHA Class I to NYHA Class II patients. No significant change was demonstrated in NYHA Class I patients as compared to Controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Modelling of passive expiration in patients with adult respiratory distress syndrome.

The time-course of volume change during passive expiration preceded by an end-inspiratory hold was studied with a biexponential model in six adult respiratory distress syndrome (ARDS) patients. We measured the initial volumes and time constants of the fast (tau 1), and the slow (tau 2) compartments of expiration, as well as the static elastance of the respiratory system. The results were compared to those of 11 normal subjects. We observed that: 1) the biexponential model fitted closely the volume decay; 2) the fast compartment was responsible for 81 +/- 7% (ARDS) versus 84 +/- 10% (controls) of the total volume exhaled, with tau 1 = 0.35 +/- 0.11 s (ARDS) versus 0.50 +/- 0.22 s (controls); 3) the slow compartment contributed only 19 +/- 6% (ARDS) versus 16 +/- 7% (controls), with tau 2 = 4.67 +/- 2.38 s (ARDS) versus 3.27 +/- 1.54 s (controls); and 4) static elastance was higher in ARDS patients. The findings could be explained in terms of a four parameter viscoelastic model of the respiratory system.

Aspirin effect on early and late changes in acute lung injury in sheep.

OBJECTIVE: There have been several studies that have already explored the potential beneficial role of cyclo-oxygenase (CO) inhibitors on oleic acid (OA)-induced lung injury in different species. These studies report no significant effect of CO inhibition, though thromboxane B2 (TxB2) was effectively blocked. However, recent studies indicate that pre-treatment with aspirin (ASA) preserve gas exchange in OA lung injury in dogs. Aim of our study has been to evaluate the potential beneficial effects of the pre-treatment with low doses of ASA on gas exchange, hemodynamics, respiratory mechanics, prostanoids and lung histology in OA-induced lung injury in sheep. DESIGN: 0.09 ml/kg of OA was administered into the right atrium of 14 anaesthetized sheep. Six received a bolus of ASA (10 mg/kg i.v.) 30 min before OA, the others saline as placebo. MEASUREMENTS AND RESULTS: Pulmonary and tissue gas exchange, pulmonary and systematic hemodynamics, respiratory system mechanics, TxB2 and 6-keto-PGF1 alpha, leukocytes and platelets concentrations were measured throughout the subsequent 3 h and lung histology was effected at end-experiment. The principal findings of our study are: 1) ASA reduces OA-induced early pulmonary vasoconstriction and bronchoconstriction, parallelled by a suppression of TxB2 generation; 2) the late increase in pulmonary artery pressure and airway resistance due to OA is not inhibited by ASA; 3) the early disturbance in pulmonary gas exchange is reduced by ASA, whereas the late severe deterioration is exaggerated by ASA; 4) the stability of tissue exchange ratio (R) at approximately 1 in ASA-group compared to its fall to approximately 0.7 in controls. CONCLUSION: Our findings suggest that ASA: 1) is only effective to treat the very transient TxB2-induced pulmonary vasoconstriction resulting in hydrostatic edema, and it is ineffective, even accentuates, the subsequent major pulmonary endothelial cell injury leading to alveolar flooding that is unrelated to TxB2; 2) has a transient protective effect on the TxB2-induced early bronchospasm; 3) has a biphasic behaviour on gas exchange, with a benefit which lasts only one hour and then results in a worse gas exchange; 4) has an immediate, stabilizing, persisting effect on R, contrasting with its transient effect on pulmonary hemodynamics and PaO2.