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Table of Contents
LETTER TO EDITOR
Year : 2021  |  Volume : 5  |  Issue : 4  |  Page : 284-285

Target and goal mismatch during mechanical ventilation in COVID-19 patients


Department of Trauma and Emergency, All India Institute of Medical Sciences, Patna, Bihar, India

Date of Submission12-Feb-2021
Date of Decision16-May-2021
Date of Acceptance20-May-2021
Date of Web Publication24-Nov-2021

Correspondence Address:
Amarjeet Kumar
Department of Trauma and Emergency, All India Institute of Medical Sciences, Patna, Bihar
India
Neeraj Kumar
Department of Trauma and Emergency, All India Institute of Medical Sciences, Patna, Bihar
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bjoa.BJOA_22_21

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How to cite this article:
Kumar A, Kumar N. Target and goal mismatch during mechanical ventilation in COVID-19 patients. Bali J Anaesthesiol 2021;5:284-5

How to cite this URL:
Kumar A, Kumar N. Target and goal mismatch during mechanical ventilation in COVID-19 patients. Bali J Anaesthesiol [serial online] 2021 [cited 2021 Nov 28];5:284-5. Available from: https://www.bjoaonline.com/text.asp?2021/5/4/284/330944



Sir,

Patients with COVID-19 pneumonia fulfilling Berlin criteria of acute respiratory distress syndrome (ARDS).[1] Severe hypoxemia in COVID-19 ARDS is mainly due to high physiological dead space, as compared to non-COVID-19 ARDS patients, leading to hypercapnia in some of the cases.[1] Some of the authors reported COVID-19 ARDS as low recruitable and improved by body positioning. Gattinoni et al.[2] proposed the existence of two primary phenotypes: Type L (low values of elastance, pulmonary ventilation/perfusion ratio, lung weight, and recruitability) and type H (high values of elastance, right-to-left shunt, lung weight, and recruitability), with the latter being more consistent with typical severe ARDS. However, the variability of the respiratory compliance is considerable, as 25% of patients have a compliance >38 ml/cm H2O, which suggests significant heterogeneity. COVID-19 virus is known for its binding capability to angiotensin-converting enzyme 2 (ACE2) receptors which are strongly expressed in endothelial cells. Infection of endothelial cells could have induced pulmonary endothelial lesions and triggered activation of coagulation cascades.

For critically ill acutely decompensated patients with COVID-19, intubation should not be delayed. It is well known that, when lung compliance is relatively normal, even more than 50% of the alveolar pressure is transmitted to the pleural pressure. Moreover, application of high positive end-expiratory pressure (PEEP) when not-needed unnecessarily increases transpulmonary pressure forcing West’s zone 3 lung regions to zones 2 and 1, leading to dead space ventilation, increasing pulmonary vascular resistance, and have a detrimental impact on hemodynamic, deteriorating venous return.[3] The Surviving Sepsis Campaign-COVID-19 guidelines and recently, the American Thoracic Society proposed to treat COVID-19 per ARDS net protocol.[4] However, there are a few issues we would like to address concerning the ventilatory strategy. The duration of mechanical ventilation is found to be prolonged in COVID-19 ARDS, when compared to other studies of ARDS.[5] It was seen that, on Day 3, there is an increase in minute ventilation and ventilatory ratio in those who died, along with a P:F ratio that failed to improve. These findings suggest the potential for differential patient trajectories within this disease. The ventilatory settings after a prolonged phase of mechanical ventilation are also challenging, as there occurs severe hypoxia and hypercapnia simultaneously despite of 100% oxygen and high minute ventilation. Hence, when we target severe hypoxia by increasing inspiratory time and PEEP, the hypercapnic phase starts, resulting in CO2 retention followed by hypercapnic renal vessels constriction that results in acute renal failure. When we target hypercapnia by increasing expiratory time and by decreasing auto-PEEP, the hypoxemia becomes more severe incompatible with life. Due to complicated pathology of COVID-19 ARDS, there is a catch-22 situation, in which the intensivist is not able to set target and goal, of hypoxemia versus hypercapnia.

Further studies are warranted for better understanding of complex gas exchange in COVID-19 would require direct measurement of the dead space and shunt fraction. As one size can’s fit all, different strategies should be applied in different phases of the disease.


  Declaration of patient consent Top


The authors certify that they have obtained all appropriate patient consent forms. In the form the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.


  Financial support and sponsorship Top


Nil.


  Conflicts of interest Top


There are no conflicts of interest.



 
  References Top

1.
Liu X, Liu X, Xu Y, Xu Z, Huang Y, Chen S, et al. Ventilatory ratio in hyper capnic mechanically ventilated patients with COVID-19-associated acute respiratory distress syndrome. Am J Respir Crit Care Med 2020;201:1297-9.  Back to cited text no. 1
    
2.
Gattinoni L, Chiumello D, Caironi P, Busana M, Romitti F, Brazzi L, et al. COVID-19 pneumonia: Different respiratory treatments for different phenotypes? Intensive Care Med 2020;46:1099-102.  Back to cited text no. 2
    
3.
Gattinoni L, Chiumello D, Rossi S. COVID-19 pneumonia: ARDS or not? Crit Care 2020;24:154.  Back to cited text no. 3
    
4.
Alhazzani W, Møller M, Arabi Y, Loeb M, Gong MN, Fan E, et al. Surviving sepsis campaign: Guidelines on the management of critically ill. Intensive Care Med 2020;28:1-34.  Back to cited text no. 4
    
5.
Bellani G, Laffey JG, Pham T, Fan E, Brochard L, Esteban A, et al. LUNG SAFE Investigators; ESICM Trials Group. Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA 2016;315:788-800.  Back to cited text no. 5
    




 

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