bronchospasmIn the three cases presented, bronchospasm was detected at the end of the bypass period, when the first attempts to inflate the lungs were accompanied by expiratory wheezing, high inflation pressures and difficulty in deflation of the lungs. Mechanical causes for wheeing include tracheobronchial obstruction, cardiac wheezing and pneumothorax. Tracheobronchial obstruction was ruled out by investigation with a fiberoptic bronchoscope. Cardiac wheezing will be accompanied by elevated left atrial pressure and alveolar edema, neither of which was noted in our patients. Although pneumothorax can produce wheezing and elevated inflation pressures, it is not likely to cause both lungs to appear overly inflated and crowd the mediastinum.

There are several possible non-mechanical etiologies of bronchospasm after cardiopulmonary bypass. One of these possibilities is activation of C3a and C5a complement anaphylatoxins during cardiopulmonary bypass. Activation of C3a and C5a complement-derived anaphylatoxins is a common occurrence during cardiopulmonary bypass, and the pump-oxygena-tor is the usual site of complement activation. High oxygen concentrations and mechanical denaturation induced by frothing in the bubble oxygenator are believed to activate the alternate (and possibly the classic) pathway. Anaphylatoxins are inflammatory mediators that stimulate the release of mast cell histamine, contract bronchial smooth muscle and increase vascular permeability. The levels of C3a and C5a complements correlate with the duration of cardiopulmonary bypass. These complement-derived inflammatory mediators have also been postulated to contribute to the pathogenesis of “post-pump syndromes.”

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