CARDIOPULMONARY EFFECTS OF CONTINUOUS POSITIVE PRESSURE VENTILATION AND INVERSED RATIO VENTILATION IN EXPERIMENTAL MYOCARDIAL-ISCHEMIA

Citation
T. Hachenberg et al., CARDIOPULMONARY EFFECTS OF CONTINUOUS POSITIVE PRESSURE VENTILATION AND INVERSED RATIO VENTILATION IN EXPERIMENTAL MYOCARDIAL-ISCHEMIA, Anasthesist, 42(4), 1993, pp. 210-220
Citations number
38
Journal title
ISSN journal
00032417
Volume
42
Issue
4
Year of publication
1993
Pages
210 - 220
Database
ISI
SICI code
0003-2417(1993)42:4<210:CEOCPP>2.0.ZU;2-C
Abstract
Continuous positive pressure ventilation (CPPV) is an established ther apy for treatment of acute respiratory failure (ARF). However, cardiac performance may be severely disturbed due to elevated intrathoracic p ressure, inducing a decrease in cardiac output (CO) and oxygen deliver y (D(O2)). Alternatively, mechanical ventilation with prolonged inspir atory to expiratory duration ratio (inversed ratio ventilation IRV) ha s been successfully used in ARF. No data are available about IRV in ac ute haemodynamic oedema. Thus, the cardiopulmonary effects of CPPV (po sitive end-expiratory pressure [PEEP] = 10 cm H2O) and IRV (inspiratio n 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 i schaemia. Methods. Continuous intravenous anaesthesia and muscle paral ysis were provided by 1.2 mg.kg-1.h-1 piritramid and 0.08 mg.kg-1.h-1 pancuronium, and the animals were ventilated with intermittent positiv e pressure ventilation (IPPV) as reference method. Cardiocirculatory p erformance was determined by means of heart rate (HR), mean arterial p ressure (MAP), mean pulmonary arterial pressure (MPAP), central venous presure (CVP), pulmonary artery occlusion pressure (PAOP) and left ve ntricular end-diastolic pressure (LVEDP). Cardiac output (CO) was dete rmined by thermodilution method. Systemic vascular resistance (SVR) wa s calculated. Pulmonary function was assessed by arterial and mixed ve nous blood gas tension for oxygen (P(aO2), P(vO2) and carbon dioxide ( P(aCO2)). Functional residual lung capacity (FRC) was measured by mean s of the foreign gas wash-in method using helium as inert gas, and det ermination of extravascular lung water (EVLW) using the thermal-dye in dicator technique. CPPV and IRV were studied in random sequence in the controlphase and 60 min after induction of acute left ventricular isc haemia, which was achieved by occlusion of the ramus interventriculari s 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 (D(O2) 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 per formance deteriorated significantly. CO decreased by 19% (P<0.05), whe reas HR, MPAP, CVP and PAOP increased (P<0.05). P(aO2) was lower (P<0. 05) and alveoloarterial P(O2) gradient (P(AaO2) increased (P<0.05). Al l animals revealed moderate pulmonary oedema (EVLW = 15.1+/-8.4 ml.kg- 1) (P<0.01) and a lower FRC. Mechanical ventilation with PEEP signific antly improved oxygenation and FRC; however, D(O2) was slightly lower than during IPPV (not significant). IRV elevated P(aO2), FRC and D(O2) , since CO was not depressed when compared with IPPV. Conclusions. CPP V and IRV may induce a recruitment of collapsed or hypoventilated lung areas, which is more pronounced during CPPV. During both modes of ven tilation, oxygenation was improved without apparent changes in EVLW Ha emodynamic performance was more impaired during CPPV, and no improveme nt of left ventricular function secondary to an elevated intrathoracic pressure was observed. Occlusion of the RIVA coronary artery typicall y induces an infarction of 35% of left ventricular muscle mass; howeve r, non-ischaemic myocardium reveals an unchanged or increased contract ility. Thus, a reduction of left ventricular preload secondary to CPPV mainly contributes to haemodynamic depression, which is less pronounc ed during IRV due to a lower peak inspiratory airway pressure and mean airway pressure. IRV may be useful for mechanical ventilation during left ventricular failure with pulmonary oedema.