High frequency ventilation (HFV) is a generic term applied to several types of ventilation: high frequency positive pressure ventilation, high frequency jet ventilation, and high frequency oscillation ventilation.
Complete discussion of the general principles of HFV and specific details of different types and applications of HFV have been detailed elsewhere. Despite mechanical differences in the delivery systems, the basic principles remain the same. Therefore, in the following discussion the term HFV will be used although specific references cited may use one of the different types of HFV.
Despite case reports, animal studies, and clinical studies involving the use of HFV in the setting of BPF, controversy still surrounds the use of HFV in patients with BPFs. The genesis of this controversy results from conflicting reports of the success of HFV in patients with BPFs. However, scrutiny of the literature reveals subgroups of patients with BPFs in whom HFV may be of clinical value and not just a “last ditch” intervention in the face of CV failure.
High frequency ventilation in animals with artificial BPFs provides clues to settings in which HFV may be useful. High frequency ventilation is generally found to be superior to CV in controlling Pco2 and Po2 in animal studies. Common to these studies are proximal (trachea or bronchial) unilateral or bilateral fistulas in the presence of presumably normal lung parenchyma. Clinical studies involving a similar BPF patient subgroup with proximal fistula and presumably normal parenchyma also show a positive response to HFV.
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More controversy surrounds the use of HFV in BPF in patients with concomitant parenchymal lung disease such as ARDS. The studies demonstrating relative efficacy of HFV in patients with proximal BPF and “normal” parenchyma also show, but to a lesser degree, some efficacy of HFV in patients with BPF and concomitant parenchymal disease. Survivorship, however, is poor in the latter subgroup, but HFV effectively normalizes gas exchange in the majority. The poor survival was attributed not to the mode of ventilation but to the patients underlying disease. Another study of patients with BPFs, in which the degree of parenchymal abnormality was unclearly defined, demonstrated efficacy and superiority of HFV in maintaining appropriate gas exchange compared with CV. Hence, this group of studies found some efficacy of HFV in patients with BPFs and concurrent parenchymal disease.
Other studies have tended not to support this concept. Seven patients having “severe pulmonary disease” and BPFs responded variably to HFV Gas exchange did not improve and fistula outflow reduction was sometimes successful; fistula flow appeared to correlate with airway pressures. A more recent study of patients with BPFs, five of seven having ARDS, compared CV and HFV while maintaining similar mean airway pressures. High frequency ventilation did not provide adequate gas exchange; a deterioration in oxygenation was noted. Mean chest tube leak (BPF leak) was not affected by HFV. The authors speculate that adequate gas exchange could be achieved during HFV using ventilator manipulations that would raise mean airway pressures. They also suggest that the probable peripheral location of BPF in patients with ARDS potentially affects fistula flow with HFV.
The variable success reported with HFV and BPF with coexisting parenchymal disease has not yet been reconciled. One can speculate that these discrepancies have their origin in differences in study design, in HFV ventilator equipment, in degrees of coexisting parenchymal disease, and in location and size of the fistulas.
difference in success using HFV in those patients with proximal BPF and normal parenchyma and those with BPF and abnormal parenchyma can be explained in part by the principles of HFV with emphasis on the role of lung parenchyma and compliance. The impedance to flow of an airway depends on three factors: (1) resistance of the airway; (2) compliance of the lung; and (3) frequency of ventilation. High frequency ventilation theoretically increases airway impedance with higher ventilation frequencies and reduces the importance of lung compliance on distribution of lung air flow. In the setting of normal lung compliance and a proximal air leak having infinite compliance (a BPF), HFV fulfills its theoretical advantage by redistributing flow to lung parenchyma and bypassing the fistula. This is achieved by increasing airway impedance and reducing the importance of lung compliance, including that of the BPF. By contrast, patients with parenchymal disease such as ARDS have poor lung compliance and BPFs arising in this setting are peripheral. High frequency ventilation is less effective in reducing fistula flow with poor lung compliance because lung compliance becomes a greater determinant of air flow than does impedance. Additionally, not just the altered parenchymal compliance but the more peripheral fistula sites in ARDS affect fistula flow and success of HFV. Bernoulli’s equation helps explain the increased fistula flow in the peripheral lesions of patients with ARDS. According to Bernoulli’s equation, during HFV lateral airway pressure is increased in more peripheral airways compared with more proximal airways. Therefore, a more peripheral airway lesion is more prone to fistula leak. Cialis Jelly
In summary, a trial of HFV appears indicated in the patient with a proximal BPF and normal lung parenchyma. It is unclear whether HFV should be considered the primary mode of ventilation in this setting. Despite discrepancies in clinical results, a trial of HFV in a critically ill patient with BPF with diffuse parenchymal disease, ie, ARDS, failing CV appears justified by the potential for success noted in the literature. Caution must be exercised, however, with close monitoring of gas exchange parameters and fistula flow whenever HFV is used in the setting of BPF.