Review of Respiratory Medicine - Volumen 22, Número 4 - December 2022

Case Reports

Extracorporeal CO2 Removal in a Patient with Status Asthmaticus who Evolved with Barotrauma

Remoción extracorpórea de CO2 en un paciente con estatus asmático que evoluciona con barotrauma

ABSTRACT

A 20-year-old male with known asthma diagnosis arrived at the Emergency Depart­ment of a hospital in his town with history of dyspnea 1 day before admission. The pa­tient then became tachycardic, tachypneic and cyanotic and received emergency intu­bation. At the ICU (Intensive care Unit) of the tertiary care general hospital, he showed severe bronchospasm, high airway pressure during mechanical ventilation (MV) and severe hypoperfusion. He received crystalloids and norepinephrine for resuscitation. On the third day, he developed subcutaneous emphysema, pneumothorax and hyper­capnia with mixed acidosis. We decided to use ultra-protective mechanical ventila­tion concomitant with Novalung^®. With this strategy, we were able to reduce airway pressures, iPEEP (intrinsic positive end-expiratory pressure) and resistive mechanical power (MP) and improve hypercapnia and acidosis. The patient was connected to Novalung^® for ten days and showed good evolution. Finally, he was extubated and discharged from the ICU, and left the hospital in good condition.

Key words: Status asthmaticus, Ventilator-induced lung injury, Extracorporeal circulation, Barotrauma

RESUMEN

Paciente varón de 20 años, con diagnóstico de asma conocida, llegó al departamento de emergencias de un hospital de su localidad con historia de disnea 1 d antes de la admisión. Posteriormente, se torna taquicárdico, taquipneico y cianótico, por lo que fue intubado de emergencia. En la UCI del hospital general de tercer nivel, presentó bron­coespasmo grave, presiones de vía aérea elevadas durante la ventilación mecánica e hipoperfusión grave. Recibió cristaloides y norepinefrina como resucitación. Al tercer día, presentó enfisema subcutáneo, neumotórax e hipercapnia con acidosis mixta. Se decidió utilizar ventilación mecánica ultraprotectora asociada con Novalung^®. Con esta estrategia, logramos reducir las presiones de la vía aérea, la PEEPi, la potencia mecánica (PM) resistiva y mejorar la hipercapnia y la acidosis. El paciente permaneció 10 d en Novalung^® y mostró buena evolución posterior. Finalmente, es extubado, dado de alta de la UCI y salió del hospital en buenas condiciones.

Palabras clave: Estado asmático, Lesión pulmonar inducida por ventilación mecánica, Circu­lación extracorpórea, Barotrauma

Received: 05/23/2022

Accepted: 09/01/2022

INTRODUCTION

It is known that mechanical ventilation (MV) produces per se injuries in the pulmonary fibrous skeleton.¹ This damage is associated with lung compliance resistance, and the adjustment of tidal volume (TV), inspiratory flow, PEEP level and respiratory rate (RR); the latter being related to the amount of times the lung is subjected to an abnormal breathing pattern per unit of time,² generating an inflammatory process with positive feedback (ventilator-induced lung injury vortex [VILI Vortex]).^{3, 4}

The status asthmaticus (SA) is developed with high airway pressures, where the resistance ele­ment is the most important one. Even though the driving pressure (DP) is not a problem, baro­trauma is also developed. In order to control the consequences of the reduction in T V and RR (hypercapnia and respiratory acidosis), an extra­corporeal CO2 remover is added (ECCO2R), which achieves decarboxylation using low blood flow and low sweep flow.^5-7

The mechanical power (MP) is divided into its three components, and the magnitude of the “resistive power” is described as being the one re­sponsible for the MP. The reduction of the RR and TV interrupts the dynamic hyperinflation cycle, thus reducing intrathoracic pressure, correcting acidosis, allowing for the attenuation of hypoxic pulmonary vasoconstriction (HPV) and reducing the postload of the right ventricle.

We present the case of an asthmatic patient with life-threatening risk who evolved with refractory hypercapnia, mixed acidosis with blood hyperten­sion and barotrauma, and was treated with arte­riovenous ECCO2R (Novalung^®).

CASE REPORT

20-year-old male with known asthma who arrived at the Emergency Service (ES) of the regional hos­pital of Antofagasta; he had been referred from To­copilla. He complained of breathing difficulty one day before admission. Then he showed tachypnea (30 rpm), with circumoral cyanosis and respiratory muscle fatigue. Due to this condition, he received orotracheal intubation and was subjected to MV deeply sedated and with neuromuscular blockade. He received norepinephrine due to the hemody­namic compromise.

He was admitted to the emergency service with an APACHE II score of 11 points. MV was first delivered via volume-controlled mode with a TV of 350 mL, RR 24, I:E ratio = 1:3, PEEP 3 cmH₂O (intrinsic PEEP = 18 cmH₂O) and FiO2 of 50%. The patient showed high inspiratory pressure (90 cmH₂ O), so nebulization with salbutamol and Berodual^® (fenoterol 0.25mg/mL + ipratropium bromide 0.5 mg/mL) was intensified. The aus­cultation revealed a bilateral decrease in breath sounds, with generalized wheezing. Respiratory monitoring showed a plateau pressure (Pplat) of 17 cmH₂O and a static compliance of 30 mL/ cmH₂O. Initial arterial blood gases: pH = 7.18, PCO₂ = 50.5 mm/Hg, PaO₂ = 89.3 mmHg, HCO3 = 18.2 mEq/L. Negative PCR test for COVID-19.

At the ICU, the patient continued with severe bronchospasm, desaturation up to 63% with in­creasing doses of noradrenaline (from 0.06 μg/kg/ min to 0.2 μg/kg/min) and hypothermia tendency. Control tests showed lactic acidosis (10.2 mMol/L) with pH of 7.17 and HCO3 of 18 mEq/L. On the third day, the subject had palpable cervical crack­ling sounds, and the chest scan showed cervical subcutaneous emphysema and pneumothorax (Figure 1). Thus, a pleural tube was placed and the ventilatory schedule was modified. Methylprednisolone boluses were included (500 mg x three times). The TV was reduced to 3.4 mL/kg of predicted body weight, RR was reduced to 10 rpm, inspiratory time to 0.72 s, minute ventilation (VE) to 2.6 L/min and the I:E ratio to 1:7, without PEEP. With this pattern, the Pmax decreased to 48 cmH₂O and the iPEEP reached 6 cmH₂ O. Due to the hypercapnia, it was associated with arte­riovenous ECCO2R (Novalung^®). Aminophylline was included. No fever or evidence of septic focus detected.

Once the patient was connected to Novalung^®, we applied the volume-controlled mode with a TV of 300 ml and a RR of 10 rpm. The Novalung^® blood flow was maintained between 1.2 L/min and 1.6 L/min, and the sweep flow was adjusted between 6 L/min and 7 L/min. Table 1 shows the PaO2/FiO2 ratio, the PaCO2 and pH on the day the Novalung^® device was connected. Twenty-four hours after being connected to Novalung^®, the maximum pressure (Pmax) of the airways was reduced and oxygenation remained unaffected. The most important modifications were a drop in the iPEEP and Pmax (Figure 1).

The patient remained connected to Novalung^® for ten days and showed good evolution. 72 h after removing the Novalung® device, the patient was extubated. Ventilatory parameters before extuba­tion: Pplat = 15 cmH₂O; DP = 10 cmH₂O; Pmax = 18 cmH₂O and MP of 10 J/min, without iPEEP. Gasometric parameters: pH = 7.44, PaCO2 = 39.6 mmHg, PaO2 = 71.9 mmHg. Give the patient’s stability, he was discharged from the ICU 120 h after extubation, having solved the bronchospasm.

DISCUSSION

The most important finding was to identify the resistive mechanical power as the leading cause of barotrauma in a patient with SA. A significant correlation was observed between the iPEEP and Pmax of the airway. Both decreased drastically when we were able to reduce the RR and TV and extend the expiratory time (I:E ratio = 1:7) after installing the Novalung^® device.

After introducing this device, the RR could be reduced from 24 rpm to 10 rpm. Thus, the iPEEP was reduced from 15 cmH₂ O to 6 cmH₂O. This change reduced pulmonary hyperinflation and probably reduced the intrathoracic pressure, im­proving venous return and cardiac output; this was reflected in the improvement of clinical perfusion, diuresis, and the correction of lactic acid. Acidosis control should reduce the HPV and postload of the right ventricle⁸ (Table 1).

When we analyzed the specific components of the MP, such as the static elastic power (associated with PEEP), the dynamic elastic power (associ­ated with TV) and the “resistive power” (native airway), we observed that the drop in the MP was caused mainly by the reduction of the resistive component, theoretically the most important one in status asthmaticus. In our case, this component reached more than 80% of the total MP on the first day (Figure 2).

When the exhalation of gas is incomplete be­cause the next inspiration begins before the lung is completely empty, air trapping occurs and the expiratory time constant (τ) may reach values near 0.9 s.9 For that reason, the expiratory time must be extended. The reduction of the TV and RR also reduced the minute ventilation (VE), which is the main cause of dynamic hyperinflation.⁹ Twenty-four hours after the installation of the Novalung^® device, we observed the impact that the reduction in the RR and the TV had on the “resistive power”, which decreased from 58 J/min to 14.6 J/min.

These patients often show increased respira­tory effort and are dehydrated, and develop lactic acidosis, worsening respiratory acidosis. All these elements were present in our patient on admission, so he received crystalloids, norepinephrine and low levels of PEEP (Table 1).

The MP considers all the elements to be in­cluded in the Otis equation. The DP and RR are the most aggressive for the pulmonary fibrous skeleton.¹⁰ On the other hand, the peak flow is also an important variable for the development of alveolar epithelial damage (Figure 3). There­fore, the decrease in the inspiratory flow avoids the disruption of the respiratory epithelium. This phenomenon has been shown in an in vitro model of Tschumperlin.¹¹ In our patient, as a consequence of the reduction in the RR, the expiratory and in­spiratory time could be simultaneously extended and so the peak flow could be reduced.

The impact of the MP has been studied in rela­tion to the acute respiratory distress syndrome (ARDS), but there aren’t enough studies that re­late it to asthmatic decompensation.^12-14 However, regardless of the specific damage patterns, the dynamic elastic power (ARDS) or resistive power (status asthmaticus), the mechanical power is inevitably transferred to the pulmonary fibrous skeleton in each mechanical cycle.

The resistive component of the MP must always be analyzed in patients with airway obstruction. When analyzing the components separately, the resistive component (grey line) clearly stands out as the main MP generator in this type of patients (Figure 2).

CONCLUSION

In short, when patients evolve with high airway pressures, despite the existence of a suitable plateau pressure, we must consider the resistive component of the MP as the origin of barotrauma (bronchial obstruction). Through simple formulas we can predict the impact of mechanical ventilator variables on asthmatic patients.¹⁰ The ECCO2R systems are a safe tool to be associated with ultra-protective MV in severe asthmatic patients.

Conflict of interest

The authors declare that there is no conflict of interest.

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