A 38-year-old male presented two-days ago with severe ARDS and was intubated on arrival. He is currently paralyzed on the following ventilator settings: Mode: VC, RR = 30, TV = 7 cc/kg IBW. His most recent ABG is: 7.25/60/70/26. How can you maximize decarboxylation (CO2 removal) and maximize lung protection in this patient?
Oxygenation is often the primary focus of healthcare professionals in patients with ARDS. However, for various reasons, decarboxylation deserves equal attention. Patients with ARDS often have increased dead space necessitating higher than normal alveolar ventilation. One of the primary goals of mechanical ventilation in early ARDS is lung protection (primarily: minimization of tidal volume). To that effect, techniques that maximize decarboxylation will facilitate lung-protective strategies.
Some of the approaches that will enhance decarboxylation in ARDS are as follows:
- Increase respiratory rate:
Increasing respiratory rate allows minimization of tidal volume. However, as tidal volume is reduced, the dead space fraction increases. In other words, for a given minute ventilation, the “alveolar ventilation” would be lower with a rapid-shallow breathing pattern (link). Beyond a certain point, increasing respiratory rate would have minimal benefit and would increase the risk of auto-PEEP.
- Minimizing apparatus dead space:
Any equipment distal to the circuit wye is responsible for this. The main culprit is heat-and-moisture exchanger (link).
- Minimizing alveolar overinflation:
Techniques that minimize alveolar overinflation will reduce alveolar dead space. This includes application of optimal PEEP and prone positioning.
- Minimizing CO2 production:
Sedation ± paralysis will reduce carbon dioxide production. Some practitioners have used hypothermia to achieve this.
- Tracheal gas insufflation:
This involves continuous or an expiratory injection of fresh gas into the central airways via an endotracheal catheter. Doing this flushes CO2 from airway dead space and thereby to decrease anatomical dead space. This technique has fallen out of favor due to technical and safety issues.
- Post-inspiratory pause:
This is a potentially useful but an underappreciated technique and deserves a separate discussion.
What is it?
Post-inspiratory pause is routinely performed manually while checking plateau pressure. However, a brief post-inspiratory pause can also be programmed to be delivered after every breath. This feature is usually available in volume control modes.
Effect of post-inspiratory pause on gas exchange
Application of a brief post-inspiratory pause after each breath enhances CO2 removal. A rather simplistic explanation of this effect is that post-inspiratory time increases the time spent by the inhaled gas in the alveoli: often referred to as mean distribution time (MDT). Since diffusion is a time-dependent process, a prolonged MDT enhances diffusion of CO2 across the blood-gas barrier.
- This strategy would be ideally used in a patient in whom the goal is to maximize lung protection and hence minimize tidal volume. This is typically not successful in an actively breathing patient.
- A longer post-inspiratory pause will maximize CO2 removal. One of the first studies on this (Devaquet et al) used 20% of total cycle time, which is a good ball park to aim for. E.g. if RR is 30, total cycle time = 2 seconds, and pause time = 0.4 seconds.
- Post-inspiratory pause increases I-time. A long I-time combined with high inspiratory rate increases the risk for developing auto-PEEP. This issue can be addressed by increasing peak flow rate and by using square (continuous) flow pattern. For a given tidal volume and peak flow rate, using square waveform halves the inspiratory flow time when compared to decelerating ramp.
- Addressing decarboxylation can be a major issue in patient with ARDS where alveolar dead space is often increased.
- In the early stage of severe ARDS where maximizing lung protection is of paramount importance, strategies that enhance decarboxylation allow minimization of tidal volume.
- Post-inspiratory pause is an underappreciated technique that can independently augment decarboxylation for a given amount of alveolar ventilation.
- Radermacher P, Maggiore SM, Mercat A. Fifty Years of Research in ARDS. Gas Exchange in Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med. 2017 Oct 15;196(8):964-984.
- Devaquet J, Jonson B, Niklason L, Si Larbi AG, Uttman L, Aboab J, Brochard L. Effects of inspiratory pause on CO2 elimination and arterial PCO2 in acute lung injury. J Appl Physiol (1985). 2008 Dec;105(6):1944-9.
- Aboab J, Niklason L, Uttman L, Brochard L, Jonson B. Dead space and CO₂ elimination related to pattern of inspiratory gas delivery in ARDS patients. Crit Care. 2012;16(2):R39.
- Sturesson LW, Malmkvist G, Allvin S, Collryd M, Bodelsson M, Jonson B. An appropriate inspiratory flow pattern can enhance CO2 exchange, facilitating protective ventilation of healthy lungs. Br J Anaesth. 2016 Aug;117(2):243-9.
- Aguirre-Bermeo, H., Morán, I., Bottiroli, M. et al. End-inspiratory pause prolongation in acute respiratory distress syndrome patients: effects on gas exchange and mechanics. Ann. Intensive Care 6, 81 (2016)
Thank you Aman for these tricks…
But is hypercapnia really a thing 😉 ?
Just a thought process – does increasing RR decrease your I time and result in poor oxygenation. I barely use VC mode on ARDS and have been using PRVC exclusively. Will appreciate your input.
Like patient with ARDS Plat pressure 41 – Obese male – Hypoxic PF ratio 90-100, not ECMO candidate – RR set at 30 + to provide MV while keeping low TV. Prone but about to lose airway. PEEP 16 FiO2 80 and PaO2 75. Wondering how would you manage this patient – APRV patient is paralyzed ?? Your input appreciated. Should I reduce RR to provide more i time and use bicarb to help with pH and use diuretic at the same time ?
Thanks a lot