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J W Biondi

Publications and source records attributed to J W Biondi.

11 recordsLinked to original sources
PubMed1992

Left ventricular diastolic function during positive end-expiratory pressure. Impact of right ventricular ischemia and ventricular interaction.

The individual and additive effects of positive end-expiratory pressure (PEEP) and right coronary artery (RCA) occlusion on left ventricular end-diastolic pressure-volume relations (LVEDPVR) were examined in six anesthetized dogs. Right ventricular (RV) and left ventricular (LV) ejection fractions (EF), end-diastolic volume (EDV) and end-systolic volumes (ESV) were measured by thermodilution as PEEP was added before and after RCA occlusion. PEEP alone caused a decline in cardiac output, transmural left atrial pressure (LAP) (6.0 +/- 0.6 to 3.2 +/- 1.4 mm Hg, p less than 0.05), and LVEDV (49 +/- 3 to 36 +/- 4 ml, p less than 0.05). RVEDV, the mean slope (+/- SD) of the LVEDPVR (0.37 +/- 0.16 to 0.30 +/- 0.19) and LAP at a common LV volume (35 ml, V35) did not change with PEEP. RCA occlusion caused cardiac output and RVEF (38 +/- 5 to 27 +/- 5%, p less than 0.05) to decline and RVESV (25 +/- 4 to 33 +/- 6 ml, p less than 0.05) to increase. RVEDV, the slope of the LVEDPVR, and LAP at V35 were unchanged from baseline. The addition of PEEP after RCA occlusion caused cardiac output to decline further. However, unlike before occlusion, there was no change in LAP (6.5 +/- 1.3 to 5.0 +/- 1.4 mm Hg) despite a decline in LVEDV (47 +/- 3 to 29 +/- 6 ml, p less than 0.05). RVESV and RVEDV increased with PEEP after RCA occlusion as did LAP at V35. The slope of the mean LVEDPVR tended to increase (0.98 +/- 1.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Hemodynamic effects of 1:2 ECG-coupled jet ventilation in the dog. A comparison with other modes.

In 16 closed-chest dogs the hemodynamics of ECG-coupled jet ventilation (JV) with frequencies of 1:1 (one breath for each cardiac systole) and 1:2 (one breath for every other cardiac systole) were compared to noncoupled JV and intermittent positive-pressure ventilation (IPPV). Cardiac output was similar during 1:2 coupling (1.6 +/- 0.2 L/min) and IPPV (1.6 +/- 0.2 L/min) but decreased during 1:1 coupling (1.2 +/- 0.2 L/min) and noncoupled JV (1.3 +/- 0.2 L/min), p less than 0.05. During 1:2 coupling and IPPV, systemic arterial and transmural left atrial pressures were increased, and pulmonary artery, pericardial, and right atrial pressures were decreased in comparison to the other JV modes. Pulmonary blood volume was preserved during 1:2 coupling but decreased during 1:1 coupling and noncoupled JV. Coupling at 1:2 preserves output by maintaining left ventricular preload via a decrease in right atrial pressure and subsequent maintenance of systemic venous return.

Airway Resistance↗
PubMed1990

Coronary flow limits right ventricular performance during positive end-expiratory pressure.

The effect of positive end-expiratory pressure (PEEP) on right ventricular performance and myocardial blood flow was determined in 16 dogs before and after right coronary artery (RCA) occlusion. Right ventricular ejection fraction (RVEF), end-diastolic volume (EDV) and end-ejection volume were measured by thermodilution. Right ventricular end-ejection pressure-volume relations (RVEEPVR) were determined at baseline and at 20 cm H2O PEEP, both before and after RCA occlusion. In four of the dogs, RVEEPVR were also determined at 10 cm H2O PEEP after RCA occlusion. With intact RCA flow, RVEF declined with PEEP (37 +/- 5 to 19 +/- 6%) with no significant change in EDV (50 +/- 11 to 42 +/- 11 ml) or end-ejection volume (31 +/- 7 to 36 +/- 9 ml). RVEEPVR and right ventricular myocardial blood flow were also unchanged with PEEP. After RCA occlusion, RVEF declined with PEEP (27 +/- 4 to 15 +/- 5%) in association with a significant increase in end-ejection volume (39 +/- 8 to 49 +/- 10 ml), but no change in EDV (53 to 55 ml). In addition, RVEEPVR and myocardial blood flow declined with RCA occlusion, and declined further with 20 cm H2O, but not with 10 cm H2O PEEP, after RCA occlusion. Therefore, in this experimental model, right ventricular performance was adversely affected during PEEP when right coronary blood flow was limited.

Animals↗
PubMed1990

Mechanical heart-lung interaction in the adult respiratory distress syndrome.

We have discussed the complex hemodynamic changes that occur throughout the respiratory cycle during spontaneous and mechanical ventilation. In patients, many cumulative factors account for the total hemodynamic burden of inspiration and expiration. Thus, the change in pleural pressure, ventilation rate, mode of ventilation, amount of spontaneous ventilation, underlying lung and cardiac disease, and intravascular volume status all affect cardiocirculatory equilibrium. In addition, in the patient with ARDS, various immune mediators that are released into the circulation will affect LV function. Knowledge of the effects discussed in this article will aid the physician in choosing therapeutic options for patients with ARDS.

Animals↗
PubMed1989

Differing responses in right and left ventricular filling, loading and volumes during positive end-expiratory pressure.

Using a combined hemodynamic and radionuclide technique, 20 patients with varied ventricular function were evaluated during positive end-expiratory pressure (PEEP) application. Left ventricular (LV) and right ventricular (RV) ejection fractions and cardiac output were measured, and ventricular volumes were derived. Seven patients (group 1) who had an increase in LV end-diastolic volume with PEEP and 13 patients (group 2) who had the more typical response, a decrease in LV end-diastolic volume with PEEP, were identified. Compared with group 2, group 1 patients had a higher incidence of coronary artery disease (5 of 7 vs 1 of 13, p less than 0.005) and lower cardiac output (3.9 +/- 1.6 vs 9.1 +/- 3.2 liters/min, p less than 0.005), LV ejection fraction (27 +/- 13 vs 51 +/- 21%, p less than 0.05), RV ejection fraction (15 +/- 6 vs 32 +/- 8%, p less than 0.005) and peak filling rate (1.32 +/- 0.43 vs 3.51 +/- 1.70 end-diastolic volumes/s, p less than 0.05). LV and RV volumes increased and peak filling rate decreased with PEEP in group 1, whereas in group 2 LV volume decreased and RV volume and peak filling rate remained unchanged. Using stepwise regression analysis, the change in LV volume with PEEP was related directly to baseline systemic vascular resistance and inversely to baseline blood pressure. Similarly, the change in peak filling rate with PEEP was inversely related to the change in RV end-diastolic volume. Thus, the hemodynamic response to PEEP is heterogeneous and may be related to LV ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Effect of positive end-expiratory pressure on right ventricular performance. Importance of baseline right ventricular function.

Thirty-six patients with diverse baseline right ventricular function were evaluated during incremental positive end-expiratory pressure (PEEP) application. Right heart pressures, cardiac output, right ventricular ejection fractions, and ventricular volumes were obtained at each PEEP level. Right ventricular peak systolic pressure-end-systolic volume relations were analyzed as an index of contractile function. Patients with severely depressed baseline right ventricular ejection fractions (30 percent or less) had an increase in end-diastolic (270 +/- 74 to 391 +/- 76 ml, 0 to 20 cm water (H2O) PEEP, p less than 0.05) and end-systolic volumes (210 +/- 70 to 321 +/- 70 ml, 0 to 20 cm H2O PEEP, p less than 0.05). These patients also had a decline in estimated right ventricular contractile function at 20 cm H2O PEEP as estimated by the slope of systolic pressure-volume relations (0.12 to 0.04 mm Hg/ml, 0 to 15 and 15 to 20 cm H2O PEEP, respectively, p less than 0.05). Patients with normal (40 percent or more) or moderately depressed (31 to 40 percent) baseline right ventricular ejection fractions had no change in right ventricular volumes or estimated contractile function. Therefore, the effect of PEEP on right ventricular function differs depending on the baseline right ventricular ejection fraction.

Adult↗
PubMed1988

The effect of incremental positive end-expiratory pressure on right ventricular hemodynamics and ejection fraction.

The effects of incremental positive end-expiratory pressure (PEEP) on right ventricular (RV) function were evaluated in 36 (n = 36) ventilated patients. Positive end-expiratory pressure was increased from 0 (baseline) to 20 cm H2O in 5-cm H2O increments and RV hemodynamics and thermally derived right ventricular ejection fraction (RVEF), right ventricular end-diastolic volume index (RVEDVI), and right ventricular end-systolic volume index (RVESVI) were computed. Right ventricular contractility was determined from the analysis of RV systolic pressure-volume relations. Right ventricular ejection fraction declined from 42 +/- 8% at baseline to 30 +/- 9% at 20 cm H2O PEEP. Right ventricular end-diastolic volume index declined between 0 and 5 cm H2O PEEP (103 +/- 42 to 92 +/- 34 ml.m-2) and then increased to 113 +/- 40 at 20 cm H2O PEEP. Right ventricular end-systolic volume index increased from 60 +/- 31 ml.m-2 at baseline to 79 +/- 34 ml.m-2 at 20 cm H2O PEEP. The slope (E) of the relation of RV peak systolic pressure to RV end-systolic volume index decreased from 0.26 mm Hg.m2.ml-1 between PEEP of 0-15 cm H2O to 0.05 mm Hg.m2.m-1 at PEEP greater than 15 cm H2O. It is concluded that low levels of PEEP have a predominant preload reducing effect on the RV. Above 15 cm H2O PEEP, RV volumes increase and E decreases, consistent with increased RV afterload and a decline in RV contractility.

Adult↗
PubMed1988

Effects of mechanical ventilation on right and left ventricular function.

We have discussed the complex hemodynamic changes that occur throughout the respiratory cycle during mechanical ventilation and have reviewed the physiologic changes associated with spontaneous respiration. In patients, many cumulative factors account for the total hemodynamic burden of mechanical inspiration and expiration. Thus, the change in pleural pressure, respiratory rate, mode of ventilation, amount of spontaneous ventilation, underlying lung and cardiac disease, and intravascular volume status all affect cardiocirculatory equilibrium during the respiratory cycle. Knowledge of the effects presented in this article will aid the physician in choosing the therapeutic options in instrumented, mechanically ventilated patients.

Cardiac Output↗
PubMed1987

Lack of association of pleural effusion with chronic pulmonary arterial and right atrial hypertension.

Right atrial hypertension has been considered to have a major physiologic influence on the formation of transudative pleural effusions. Since pleural fluid is thought to be cleared primarily by the parietal pleural lymphatic vessels that empty into the systemic veins, systemic venous hypertension secondary to right atrial hypertension should decrease the lymphatic drainage of the pleural space. We retrospectively studied nine patients and prospectively studied 18 patients with long-term right atrial or pulmonary arterial hypertension (or both). All patients had stable respiratory symptoms, and none had a significantly elevated pulmonary arterial wedge pressure. Our purpose was to determine the relationship of right atrial and pulmonary arterial hypertension to the development of transudative pleural effusions. Posteroanterior and bilateral decubitus chest roentgenograms and ultrasound were used to detect pleural effusions. Pleural effusions were not identified in any of the 27 patients, even in four patients with right atrial pressures greater than 20 mm Hg. We conclude that chronic elevation of right atrial pressure or pulmonary arterial pressure (or both) alone is not a cause of pleural effusion. In contrast, elevation of left atrial and pulmonary arterial wedge pressures is associated with the formation of transudative pleural effusions in man. Thus, if pleural effusions are detected in patients who have cor pulmonale, a search should be made for coexisting left heart failure or a primary cause of pleural inflammation, such as pulmonary emboli or infection.

Blood Pressure↗
PubMedDate not supplied

The adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) represents a common denominator of acute lung injury leading to alveolar flooding, decreased lung compliance, and altered gas transport. In the absence of specific etiology and therapy, the management of ARDS remains largely supportive. Ubiquitous use of intermittent positive-pressure ventilation with positive end-expiratory pressure (PEEP) improves arterial oxygenation but with some risk of pulmonary barotrauma and decreased cardiac output. The recent understanding of lung inflation as a modulator of right heart afterload and the effect of the right ventricle on global cardiac performance continues to redefine optimal patterns of ventilatory and hemodynamic intervention in ARDS.

Capillary Permeability↗