Hachenberg T, Meyer J, Sielenkämper A, Kraft W, Vogt B, Breithardt G, Lawin P
Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Westfälische Wilhelms-Universität Münster.
Anaesthesist. 1993 Apr;42(4):210-20.
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
持续正压通气(CPPV)是治疗急性呼吸衰竭(ARF)的一种既定疗法。然而,由于胸内压升高,心脏功能可能会受到严重干扰,导致心输出量(CO)和氧输送(DO2)降低。另外,延长吸气与呼气时间比的机械通气(反比通气IRV)已成功用于ARF的治疗。目前尚无关于急性血流动力学水肿中IRV的相关数据。因此,我们在9只犬(体重29.9±4.3kg)身上研究了心肌缺血诱导前后CPPV(呼气末正压[PEEP]=10cmH2O)和IRV(吸气与呼气时间比[I:E]=3.0)对心肺的影响。方法:通过静脉持续输注1.2mg·kg-1·h-1的匹莫林和0.08mg·kg-1·h-1的泮库溴铵进行持续静脉麻醉和肌肉松弛,动物采用间歇正压通气(IPPV)作为对照方法进行通气。通过心率(HR)、平均动脉压(MAP)、平均肺动脉压(MPAP)、中心静脉压(CVP)、肺动脉闭塞压(PAOP)和左心室舒张末期压力(LVEDP)来测定心脏循环功能。通过热稀释法测定心输出量(CO)。计算全身血管阻力(SVR)。通过动脉和混合静脉血中氧(PaO2、PvO2)和二氧化碳(PaCO2)的血气张力评估肺功能。使用氦气作为惰性气体,通过外源性气体冲洗法测量功能残气量(FRC),并使用热染料指示剂技术测定血管外肺水(EVLW)。在对照期和急性左心室缺血诱导后60分钟,以随机顺序研究CPPV和IRV,急性左心室缺血通过闭塞前室间支实现。结果:在对照期,CPPV导致MPAP(P<0.05)、CVP(P<0.05)和PAOP(P<0.05)升高。HR和MAP保持不变,而CO降低了16%(P<0.05)。FRC升高了25ml·kg-1(P<0.01),但EVLW未升高(9.1±3.5ml·kg-1)。氧合没有改善;相反,氧输送(DO2)降低(P<0.05)。在反比通气期间,MPAP、CVP、PAOP升高,但低于CPPV期间。FRC升高了7.0ml·kg-1(P<0.05),显著低于CPPV期间(P<0.05)。EVLW无差异。在缺血期IPPV期间,心肺功能显著恶化。CO降低了19%(P<0.05),而HR、MPAP、CVP和PAOP升高(P<0.05)。PaO2降低(P<0.05),肺泡-动脉氧分压差(PAaO2)升高(P<0.05)。所有动物均出现中度肺水肿(EVLW=15.1±8.4ml·kg-1)(P<0.01),FRC降低。使用PEEP的机械通气显著改善了氧合和FRC;然而,DO2略低于IPPV期间(无显著差异)。IRV提高了PaO2、FRC和DO2,因为与IPPV相比,CO未降低。结论:CPPV和IRV可能会使塌陷或通气不足的肺区域复张,在CPPV期间这种情况更明显。在两种通气模式下,氧合均得到改善,而EVLW无明显变化。CPPV期间血流动力学性能受损更严重,未观察到因胸内压升高导致的左心室功能改善。闭塞RIVA冠状动脉通常会导致35%的左心室肌肉质量梗死;然而,非缺血心肌的收缩力保持不变或增加。因此,CPPV导致的左心室前负荷降低主要导致血流动力学抑制,由于吸气气道峰值压力和平均气道压力较低,IRV期间这种情况不太明显。IRV可能对机械通气有用。