In mechanically ventilated patients with acute circulatory failure related to sepsis, we investigated whether the respiratory changes in arterial pressure could be related to the effects of volume expansion (VE) on cardiac index (CI). Forty patients instrumented with indwelling systemic and pulmonary artery catheters were studied before and after VE. Maximal and minimal values of pulse pressure (Ppmax and Ppmin) and systolic pressure (Psmax and Psmin) were determined over one respiratory cycle. The respiratory changes in pulse pressure (Δ Pp) were calculated as the difference between Ppmax and Ppmin divided by the mean of the two values and were expressed as a percentage. The respiratory changes in systolic pressure (Δ Ps) were calculated using a similar formula. The VE-induced increase in CI was ⩾ 15% in 16 patients (responders) and < 15% in 24 patients (nonresponders). Before VE, Δ Pp (24 ± 9 versus 7 ± 3%, p < 0.001) and Δ Ps (15 ± 5 versus 6 ± 3%, p < 0.001) were higher in responders than in nonresponders. Receiver operating characteristic (ROC) curves analysis showed that Δ Pp was a more accurate indicator of fluid responsiveness than Δ Ps. Before VE, a Δ Pp value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 94% and a specificity of 96%. VE-induced changes in CI closely correlated with Δ Pp before volume expansion (r2 = 0.85, p < 0.001). VE decreased Δ Pp from 14 ± 10 to 7 ± 5% (p < 0.001) and VE-induced changes in Δ Pp correlated with VE-induced changes in CI (r2 = 0.72, p < 0.001). It was concluded that in mechanically ventilated patients with acute circulatory failure related to sepsis, analysis of Δ Pp is a simple method for predicting and assessing the hemodynamic effects of VE, and that Δ Pp is a more reliable indicator of fluid responsiveness than Δ Ps.

In ventilated patients with acute lung injury (ALI) we investigated whether respiratory changes in arterial pulse pressure ( Δ PP) could be related to the effects of PEEP and fluid loading (FL) on cardiac index (CI). Measurements were performed before and after application of a PEEP (10 cm H2O) in 14 patients. When the PEEP-induced decrease in CI was > 10% (six patients), measurements were also performed after FL. Maximal (PPmax) and minimal (PPmin) values of pulse pressure were determined over one respiratory cycle and Δ PP was calculated: Δ PP (%) = 100 × {(PPmax − PPmin)/ ([PPmax + PPmin]/2)}. PEEP decreased CI from 4.2 ± 1.1 to 3.8 ± 1.3 L/min/m2 (p < 0.01) and increased Δ PP from 9 ± 7 to 16 ± 13% (p < 0.01). The PEEP-induced changes in CI correlated with Δ PP on ZEEP (r = − 0.91, p < 0.001) and with the PEEP-induced increase in Δ PP (r = − 0.79, p < 0.001). FL increased CI from 3.5 ± 1.1 to 4.2 ± 0.9 L/min/m2 (p < 0.05) and decreased Δ PP from 27 ± 13 to 14 ± 9% (p < 0.05). The FL-induced changes in CI correlated with Δ PP before FL (r = 0.97, p < 0.01) and with the FL-induced decrease in Δ PP (r = − 0.85, p < 0.05). In ventilated patients with ALI, Δ PP may be useful in predicting and assessing the hemodynamic effects of PEEP and FL.

There is growing recognition of the clinical importance of pulmonary haemodynamics during exercise, but several questions remain to be elucidated. The goal of this statement is to assess the scientific evidence in this field in order to provide a basis for future recommendations.Right heart catheterisation is the gold standard method to assess pulmonary haemodynamics at rest and during exercise. Exercise echocardiography and cardiopulmonary exercise testing represent non-invasive tools with evolving clinical applications. The term “exercise pulmonary hypertension” may be the most adequate to describe an abnormal pulmonary haemodynamic response characterised by an excessive pulmonary arterial pressure (PAP) increase in relation to flow during exercise. Exercise pulmonary hypertension may be defined as the presence of resting mean PAP 30 mmHg during exercise with total pulmonary resistance >3 Wood units. Exercise pulmonary hypertension represents the haemodynamic appearance of early pulmonary vascular disease, left heart disease, lung disease or a combination of these conditions. Exercise pulmonary hypertension is associated with the presence of a modest elevation of resting mean PAP and requires clinical follow-up, particularly if risk factors for pulmonary hypertension are present. There is a lack of robust clinical evidence on targeted medical therapy for exercise pulmonary hypertension.

Pulmonary hypertension is characterised by the chronic elevation of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) leading to right ventricular enlargement and hypertrophy. Pulmonary hypertension may result from respiratory and cardiac diseases, the most severe forms occurring in thromboembolic and primary pulmonary hypertension.Pulmonary hypertension is most often defined as a mean PAP >25 mmHg at rest or >30 mmHg during exercise, the pressure being measured invasively with a pulmonary artery catheter. Doppler echocardiography allows serial, noninvasive follow-up of PAPs and right heart function. When the adaptive mechanisms of right ventricular dilatation and hypertrophy cannot compensate for the haemodynamic burden, right heart failure occurs and is associated with poor prognosis.The haemodynamic profile is the major determinant of prognosis. In both primary and secondary pulmonary hypertension, special attention must be paid to the assessment of pulmonary vascular resistance index (PVRI), right heart function and pulmonary vasodilatory reserve.Recent studies have stressed the prognostic values of exercise capacity (6-min walk test), right atrial pressure, stroke index and vasodilator challenge responses, as well as an interest in new imaging techniques and natriuretic peptide determinations. Overall, careful haemodynamic evaluation may optimise new diagnostic and therapeutic strategies in pulmonary hypertension.