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|Pressure controlled inverse ratio ventilation in acute respiratory distress syndrome patients|
Year : 2002 | Volume : 48 | Issue : 1 | Page : 34-6
M Tripathi, RK Pandey, S Dwivedi
Correspondence Address: M Tripathi
Mechanical ventilation still remains the main stay in the management of the acute respiratory distress syndrome (ARDS). High tidal volume and high airway pressure lead to lung barotrauma and the morbidity hence, there is need to use alternative modes of ventilation. Pressure control with inverse ratio ventilation (PC-IRV) has been extensively studied in recent past.,,, Contradictory claims regarding its efficiency have been reported in different studies on animal, and in human.,, The indications to start PC-IRV and to terminate it are still not very clear. We wish to share our experience of two patients, who required completely different modes of ventilation inspite of similar clinical presentation.
At the time of admission heart rate was 108/min and blood pressure of 120/60 mmHg. She was semiconscious; responding to painful stimuli, Glasgow coma scale (GCS) of 6, and normal reacting pupils. Deep tendon reflexes were depressed and the plantar reflex was flexor. While the patient was breathing room air, the arterial oxygen saturation (SaO2) was 86%. The radiograph of chest showed diffuse bilateral infiltrates in all the quadrants. ECG revealed a normal sinus rhythm. A probable diagnosis of cerebral malaria/viral encephalitis was made and patient was given quinine, mannitol, dexamethasone and phenytoin. In addition, she received ceftriaxone, metronidazole, ranitidine, aminophylline infusion and oxygen (5l/min) by facemask.
Second day, she developed hypotension, respiratory distress, and fall in SaO2 from 96% to 78%. Coarse crepitations and scattered ronchi were heard bilaterally. At this time, dopamine infusion was started, tracheal intubation was done and ventilatory assistance was provided (SIMV-10, tidal volume (VT)-500ml, I:E-1:2, FIO2-0.8, CPAP-7cmH2O and ASB 20cmH2O). With this mode, her SaO2 deteriorated to 70%, after 4 hours and the FiO2 was increased to 1.00. The chest radiograph revealed ill defined blotchy opacities in the middle and lower zones with air-bronchogram corresponding to extensive intra-alveolar pulmonary oedema and lung injury score (LIS) 2.7 and APACHI-II 26 [Table]. Arterial blood gases analysis showed pH 7.32, PaO2 56mmHg and PaCO2 28mmHg. Haematological and other laboratory values were suggestive of septic shock. The patient was pharmacologically paralysed and volume controlled IPPV was instituted. This restored the SaO2 to 90%.
Third day morning, the SaO2 again dropped to 74% at FiO2 1.00 and arterial blood gases showed further deterioration pH 7.16; PaO2 64mmHg; PaCO2 23mmHg. At this time peak inspiratory pressure (PIP) was as high as to 62 cmH2O for the ventilator setting (VT-500ml, RR-15 I:E-1:2) and monitored total dynamic compliance 14ml/cmH2O and resistance-21cmH2O/ml. Tachycardia (heart rate-178bpm), hypotension (ABP-79/41mmHg) was noted. It was decided to change the ventilator mode to PC-IRV. The ventilator settings were Pmax 30cmH20, RR 15/min, VT 500ml, PEEP 10cmH20, FiO2 1.00, I:E-3:1. This mode of ventilation improved oxygenation at FiO2 1.00; SaO2 97%; PaO2 74mmHg and pH 7.14 and PaCO2 32mmHg. Haemodynamically, she improved as well (ABP-106/67mmHg and heart rate-137bpm). Dobutamine and adrenaline infusions were also started along with the renal dose of dopamine. Suitable antibiotics were started on the basis of blood culture report.
On day four, her condition facilitated reduction of FiO2 to 0.5 in next 20 hours of starting of PC-IRV to attain SaO2 97%; PaO2 94mmHg; pH 7.3, and it was decided to discontinue muscle relaxant, change the ventilator mode to SIMV (RR 10/min; VT 500ml) and ASB 20cmH2O with normal I:E ratio (1:2). Within two hours of it, the oxygenation of the patient deteriorated (PaO2 58mmHg; SaO2 74%) and the FiO2 was increased back to 0.9. Patient developed frank pulmonary oedema and coarse crepitations. At this time, we noted that the compliance was still very low (10ml/cmH2O) with high resistance (21cmH2O/ml). The ventilator mode was reverted back to PC-IRV, and continued for the next 36 hours. After this time, when compliance improved to 28ml/cmH2O and resistance to 14cmH2O/ml to get VT 500ml, the ventilation could be changed to SIMV with ASB successfully. Over next four days the patient could be successfully weaned from the ventilator and was extubated.
Second day, the patient became extremely restless and violent with irrelevant talking. Clinically, patient was showing cyanosis and tachypnoea (RR>50/min). It was decided to start elective positive pressure ventilation and accordingly patient was sedated with midazolam (8mg IV) and muscle relaxation with vecuronium (8mg). Nasotracheal intubation was done. IPPV was started at FiO2 0.60 (tidal volume 650ml; RR 12/min). Arterial blood gas analysis 20min later revealed (PaO2 48mmHg; pH 7.02; and PaCO2 18mmHg). FiO2 was increased to 1.00 and sodium bicarbonate (7.5%) 100ml was given in slow infusion. Immediate X-ray chest showed diffuse bilateral infiltrates in all the quadrants, LIS 2.7 and APACHI II 32 [Table]. ECG revealed a normal sinus rhythm.
Third day, during conventional mode of ventilation (tidal volume 10ml/kg; respiratory rate 12/min), PIP was 42cmH2O, dynamic lung compliance 34ml/cmH2O, airway resistance 13cmH2O/ml. Her ABP ranged (70-75mmHg) and heart rate (136-149bpm) with inotropic support (Dopamine-10mcg/kg/min) but to maintain SaO2 88%, PaO2 (64mmHg), we had to keep FiO2 1.00. To improve oxygen saturation at safer FiO2 (<0.6) limits, we tried to increase PEEP 15cmH2O but this did not improve the oxygenation and it was decided to try PC-IRV (PC 30cmH2O; VT 500ml, I:E 3:1; and RR-12/min). At this ventilator setting, patient desaturated (SaO2 74%) in place of expected improvement. ABP showed marginal improvement (mean 80mmHg) but we had to abandon the PC-IRV setting and started again the conventional ventilation with PEEP 15cmH2O and tidal volume (10ml/kg). Arterial blood gas improved gradually to pH-7.32, PaO2 102mmHg at FiO2 0.9 and PaCO2 36mmHg. Patient continued to improve with conventional mode of ventilation gradually.
In first patient, PC-IRV worked well to improve oxygenation and haemodynamics. Here, the patient had significantly low dynamic lung compliance (9ml/cmH2O), high PIP (>60cmH2O) during I:E/1:2 ventilation at VT (10ml/kg) and the hypotension even on inotropic support. After starting PC-IRV, her mean ABP improved to 68mmHg. Adrenaline infusion helped to maintain mean ABP above 75mmHg. PC-IRV in this patient improved ventilation as well.
In second patient, where during conventional mode of ventilation (VT 10ml/kg; RR 12/min), although PIP (42cmH2O) was high, but the dynamic compliance (34ml/cmH2O) was better. Patient was maintaining mean ABP at 70-75mmHg and heart rate (136-149bpm) with inotropic support, and oxygenation (SaO2 88%; PaO2 64mmHg at FiO2 1.0), and PaCO2 (36mmHg). To get oxygenation at safe FiO2 limits (<0.60), we tried to increase PEEP from 7 to 15cmH2O, but when this failed, we decided to try PC-IRV (PC 30cmH2O; VT 500ml; I:E 3:1; and RR 12/min). On PC-IRV, patient developed desaturation to (SaO2 74%) in place of expected improvement. ABP improved marginally (mean ABP 80mmHg) and we abandoned the PC-IRV setting after a trial for 30min and started again the conventional ventilation with PEEP 15cmH2O, VT 10ml/kg, and I:E 1:2 with improvement.
Although PC-IRV has been reported with increased PaCO2,, and low cardiac output but we found a definite improvement in first patient in terms of decreased PIP, and better oxygenation, while did not show any change in second patient. These two patients point out that probably the low dynamic lung compliance (<20ml/cmH2O), high PIP (>50cmH2O) at conventional I:E ratio (1:2), tidal volume setting (10ml/kg), hypotension and low acute lung injury score (<2.7) should form a basis to develop a scoring system to help guide us as to when to switch over PC-IRV ventilation.
In summary, with this experience, we wish to highlight that it is not uncommon to find two patients of similar clinical picture requiring different ventilation strategy in ARDS. We need to tailor various modes of ventilation depending upon individual patient’s response and his clinical condition, to achieve goals of ventilation. PC-IRV is still a mode of ventilation benefiting in extreme conditions of ARDS and rigorous clinical trials are required to establish the appropriate time of its initiation or termination, and the correct patient selection to get the benefit of PC-IRV in ARDS subjects.