Continuous positive pressure ventilation (CPPV) is an established therapy for treatment of acute respiratory failure (ARF). However, cardiac performance may be severely disturbed due to elevated intrathoracic pressure, inducing a decrease in cardiac output (CO) and oxygen delivery (DO2). Alternatively, mechanical ventilation with prolonged inspiratory to expiratory duration ratio (inversed ratio ventilation IRV) has been successfully used in ARF. No data are available about IRV in acute haemodynamic oedema. Thus, the cardiopulmonary effects of CPPV (positive end-expiratory pressure [PEEP] = 10 cm H2O) and IRV (inspiration to expiration duration ratio [I:E] = 3.0) were studied in nine dogs (body weight 29.9 +/- 4.3 kg) before and after induction of myocardial ischaemia. METHODS. Continuous intravenous anaesthesia and muscle paralysis were provided by 1.2 mg.kg-1 x h-1 piritramide and 0.08 mg.kg-1 x h-1 pancuronium, and the animals were ventilated with intermittent positive pressure ventilation (IPPV) as reference method. Cardiocirculatory performance was determined by means of heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and left ventricular end-diastolic pressure (LVEDP). Cardiac output (CO) was determined by thermodilution method. Systemic vascular resistance (SVR) was calculated. Pulmonary function was assessed by arterial and mixed venous blood gas tension for oxygen (PaO2, PvO2) and carbon dioxide (PaCO2). Functional residual lung capacity (FRC) was measured by means of the foreign gas wash-in method using helium as inert gas, and determination of extravascular lung water (EVLW) using the thermal-dye indicator technique. CPPV and IRV were studied in random sequence in the control phase and 60 min after induction of acute left ventricular ischaemia, which was achieved by occlusion of the ramus interventricularis anterior. RESULTS. During the control phase CPPV induced an increase in MPAP (P < 0.05), CVP (P < 0.05) and PAOP (P < 0.05). HR and MAP remained unchanged, whereas CO decreased by 16% (P < 0.05). FRC was elevated by 25 ml.kg-1 (P < 0.01), but not EVLW (9.1 +/- 3.5 ml.kg-1). There was no improvement in oxygenation; instead, oxygen delivery (DO2) decreased (P < 0.05). During inversed ratio ventilation MPAP, CVP, PAOP increased, but less than during CPPV. FRC was elevated mu 7.0 ml.kg-1 (P < 0.05), which was significantly less than during CPPV (P < 0.05). EVLW revealed no differences. During IPPV in the ischaemia phase cardiopulmonary performance deteriorated significantly. CO decreased by 19% (P < 0.05), whereas HR, MPAP, CVP and PAOP increased (P < 0.05). PaO2 was lower (P < 0.05) and alveolo-arterial PO2 gradient (PAaO2) increased (P < 0.05). All animals revealed moderate pulmonary oedema (EVLW = 15.1 +/- 8.4 ml.kg-1) (P < 0.01) and a lower FRC. Mechanical ventilation with PEEP significantly improved oxygenation and FRC; however, DO2 was slightly lower than during IPPV (not significant). IRV elevated PaO2, FRC and DO2, since CO was not depressed when compared with IPPV. CONCLUSIONS. CPPV and IRV may induce a recruitment of collapsed or hypoventilated lung areas, which is more pronounced during CPPV. During both modes of ventilation, oxygenation was improved without apparent changes in EVLW. Haemodynamic performance was more impaired during CPPV, and no improvement of left ventricular function secondary to an elevated intrathoracic pressure was observed. Occlusion of the RIVA coronary artery typically induces an infarction of 35% of left ventricular muscle mass; however, non-ischaemic myocardium reveals an unchanged or increased contractility. Thus, a reduction of left ventricular preload secondary to CPPV mainly contributes to haemodynamic depression, which is less pronounced during IRV due to a lower peak inspiratory airway pressure and mean airway pressure. IRV may be useful for mechanical ventCntCo