Mechanical ventilation in patients with acute ischaemic stroke: from pathophysiology to clinical practice

Abstract

Most patients with ischaemic stroke are managed on the ward or in specialty stroke units, but a significant number requires higher-acuity care and, consequently, admission to the intensive care unit. Mechanical ventilation is frequently performed in these patients due to swallowing dysfunction and airway or respiratory system compromise. Experimental studies have focused on stroke-induced immunosuppression and brain-lung crosstalk, leading to increased pulmonary damage and inflammation, as well as reduced alveolar macrophage phagocytic capability, which may increase the risk of infection. Pulmonary complications, such as respiratory failure, pneumonia, pleural effusions, acute respiratory distress syndrome, lung oedema, and pulmonary embolism from venous thromboembolism, are common and found to be among the major causes of death in this group of patients. Furthermore, over the past two decades, tracheostomy use has increased among stroke patients, who can have unique indications for this procedure—depending on the location and type of stroke—when compared to the general population. However, the optimal mechanical ventilator strategy remains unclear in this population. Although a high tidal volume (VT) strategy has been used for many years, the latest evidence suggests that a protective ventilatory strategy (VT = 6–8 mL/kg predicted body weight, positive end-expiratory pressure and rescue recruitment manoeuvres) may also have a role in brain-damaged patients, including those with stroke. The aim of this narrative review is to explore the pathophysiology of brain-lung interactions after acute ischaemic stroke and the management of mechanical ventilation in these patients.

Ventilation time and prognosis after stroke thrombectomy: the shorter, the better!

“…The majority of sedative drugs can cause hypotension, which might negatively affect cerebral blood flow in the critical time period after recanalization, possibly influencing final infarct size. Additionally, hyperoxaemia may be present for a longer time in patients with delayed extubation, which might contribute to secondary brain injury and worse outcomes [15,16]. Furthermore, early diagnostic stroke workup may be impeded in patients who remain intubated for a longer time, potentially leading to delays in specific treatment of stroke causes.…”

“…The majority of patients had an M1-segment occlusion of the middle cerebral artery (65.3%); 58.6% had been treated with intravenous thrombolysis before MT. Median National Institutes of Health Stroke Scale (NIHSS) at admission was 15 (interquartile range [11][12][13][14][15][16][17][18] and successful recanalization (thrombolysis in cerebral infarction grades 2b-3) was achieved in 88.5% of the patients (Table 1).…”

Mechanical ventilation and neurocritical patients: is there a role for anti-neuroinflammatory therapies?

“…Battaglini D; Bonatti G; Robba C; Rocco PRM; Pelosi P Dear Editor, We thank Professor Bilotta and colleagues for their interest in our recent scientific contribution [1]. The authors pointed out the role of neuroinflammation due to mechanical ventilation in stroke, thus advising the relevance of possible novel pharmacological strategies.…”

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read with great attention and interest the review by Robba and colleagues on mechanical ventilation (MV) in patients with acute ischemic stroke [1].The authors examined the pathophysiology of stroke and the risk for pulmonary complications (brain-lung "dangerous" crosstalk, immunological response after stroke, stroke-associated pneumonia, and dysphagia) then concluding with useful recommendations on optimal ventilator settings and therapeutic strategies.Several preclinical evidence supports that MV correlates with neuroinflammation and cognitive dysfunction [2,3].Surprisingly the authors in their review cite a paper from Hegeman and colleagues that challenge the hypothesis of the relationship between MV and brain inflammation state: "In the brain, MV did not induce a significant change in adhesion molecule mRNA expression as compared with non-ventilated controls, […] did not induce a detectable cytokine or chemokine response, [...] myeloperoxidase activity was below detection level in all experimental groups" [4].Of interest, the study from Klinger and colleagues reported evidence on the effect of intravenous lidocaine on the transcerebral inflammatory response during cardiac surgery [5]. In their randomized controlled clinical trial, the authors aimed to investigate the potential antineuroinflammatory effect of intravenous lidocaine and observed "a reduction in the transcerebral activation of platelet-monocyte conjugates after aortic cross-clamp release.

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“…We read with great attention and interest the review by Robba and colleagues on mechanical ventilation (MV) in patients with acute ischemic stroke [1].…”