Cardiovascular effects of high frequency ventilation - the possible involvement of thromboxane

Recent studies with high frequency ventilation (HFV) have noted that HFV-induced increases in mean airway pressure leads to a marked cardiovascular depression, especially in cardiac output (CO).Aside from mechanical events a negative inotropic agent possibly prostaglandin in nature may also be involved. This study examined the possible involvement of thromboxane A₂ (TXA₂) in the HFV-induced cardiovascular deterioration. Chloralose-anesthetized mechanically-ventilated dogs were subjected to HFV 4, 10, and 20 mm Hg for 30 min. Some animals were also treated with imidazole (25 mg/Kg/hr) prior to HFV. Arterial levels of TXB₂ (stable metabolite of TXA₂) where monitored by radioimmunoassay. During HFV, tracheal pressure-related decreases in both CO and stroke volume (SV) were noted. Imidazole treatment significantly reduced the decrement in SV. Application of HFV resulted in variable changes in circulating TXB₂ levels. Overall, application of HFV did not result in a significant change from baseline levels.Furthermore there was no correlation between changes in CO and SV with changes in arterial TXB₂ concentration. These results do not support the hypothesis that hyperexpansion of the lungs during HFV causes the release of a cardiodepressant prostanoid.