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 (V_T) strategy has been used for many years, the latest evidence suggests that a protective ventilatory strategy (V_T = 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.

Keywords: Brain injury; Brain-lung crosstalk; Intensive care unit; Mechanical ventilation; Stroke.

Fig. 1

Brain-systemic crosstalk. After stroke, stimulation of the vagus nerve through nicotinic acetylcholine receptor α7 (nAChRα7) induces microglial activation, causing reduced alveolar macrophage phagocytic capability and reducing circulating levels of interleukin IL-6 and tumour necrosis factor TNF-α, thus leading to an anti-inflammatory reflex and lung injury. On the other hand, systemic inflammation consequent to stroke leads to an increased release of inflammatory mediators such as IL-6 and TNF-α, resulting in lung inflammation and alveolar-capillary injury. Finally, a sympathetic response with increased expression of inflammatory mediators and hypothalamic-pituitary-adrenal axis activation induces elevated glucocorticoid secretion, which might be associated with secondary infections and poor outcome

Fig. 2

The role of the vagal pathways in the development of lung injury. The healthy brain can control excess cytokine production via an inflammatory reflex of the vagus nerve (by activation of the afferent vagus through the celiac ganglion). Stimulation of the vagus nerve through nicotinic acetylcholine receptor α7 (nAChRα7) regulates microglial activation in the brain, protects neuronal cells from oxidative stress, and improves functional recovery, contributing to immunosuppression. Expression of nAChRα7 on alveolar macrophages and epithelial cells induces a reduction of inflammation in the lungs, and, by suppressing the production of pro-inflammatory cytokines (IL-6, TNF-α) through lipopolysaccharides (LPS) and nuclear factor kappa-light-chain-enhancer of activated B cells (NFK-B), impairs host defence during inflammatory conditions. Altogether, vagal stimulation during stroke blunts macrophage capabilities, with increased risk of infection and lung injury, while paradoxically inducing a higher anti-inflammatory response and thus decreasing the risk of lung injury. The balance between these two pathways accounts for the occurrence, or not, of lung injury. Ach, acetylcholine; NA, noradrenaline

Fig. 3

Recommended mechanical ventilation strategies for patients with acute ischaemic stroke. Abbreviations: PEEP, positive end-expiratory pressure; O₂, oxygen; CO₂, carbon dioxide