Tension pneumothorax is variously defined but is generally thought of as a pneumothorax in which the pressure of intrapleural gas exceeds atmospheric pressure, producing adverse effects, including mediastinal shift associated with cardiovascular collapse, often attributed to reduced venous return and kinking of the great vessels. The mechanism of tension pneumothorax is said to be a valvular defect in the visceral pleura such that air enters the pleural space in inspiration but cannot exit in expiration, leading to a progressive increase in pressure. However, as the driving pressure forcing air into the pleura in inspiration is atmospheric pressure, the pleural pressure can never exceed 1 atm during inspiration in a spontaneously breathing subject. Furthermore, all pneumothoraces must have pressures greater than atmospheric during expiration, or conventional treatment with intercostal tube drainage would not work. Pilot experiments have failed to show any re-entry of pleural gas into the lung in patients with persistent air leaks but no evidence of tension, suggesting these behave as valvular pneumothoraces. Case reports of tension pneumothorax in spontaneously breathing patients are rare, and most patients have other explanations for clinical deterioration. Although a large and rapidly expanding pneumothorax may require urgent intervention, it is unlikely that the effects are mediated by high intrapleural pressures. The term tension pneumothorax in spontaneously breathing patients should be reconsidered.
Dear Editor:We read with interest your recent article on 'Acute haemodynamic effects of continuous positive airway pressure in awake patients with heart failure' and the related editorial. 1,2 As the editorial points out, continuous positive airway pressure (CPAP) could theoretically have deleterious effects on cardiac function by reducing venous return and filling pressure but has in fact been shown to be beneficial in dilated cardiomyopathy presumably as a consequence of reducing left ventricular transmural pressure. In pure diastolic heart failure, both the reduced filling pressure and reduction in transmural pressure could have potential deleterious effects. We have studied five patients with pure diastolic heart failure defined as having one episode of clinical heart failure, normal systolic function (i.e. EF > 60%) on transthoracic echocardiography and an abnormal diastolic filling pattern on Doppler echocardiography with at least three of either: an early filling velocity to late filling velocity ratio (E:A) less than 1.0, a mitral deceleration time >240 msec, an isovolumic relaxation time >90 msec or a colour M-mode propagation velocity <40 msec. Additionally, they needed to have two-dimensional echocardiographic appearances consistent with diastolic dysfunction, that is left atrial dilatation and/or left ventricular hypertrophy.We assessed for a change in cardiac function and the effect of CPAP at 10 cm of water using these echocardiographic criteria, with measurements taken at 2 and 5 min post-application of CPAP, and the mean of the two readings compared with the baseline reading.Of the five patients studied, no patient demonstrated a statistically significant change with the application of CPAP in the measured echocardiographic parameters.In this small group of patients, we did not demonstrate a significant deleterious effect of nasal CPAP on diastolic cardiac function but we feel that more sophisticated assessment of cardiac function by such things as advanced echocardiographic techniques may be useful in disentangling the effects of CPAP in heart failure and provide more information than simply measuring blood pressure changes.
REFERENCES1 Schroll S, Sériès F, Lewis K, Benjamin A, Escourrou P, Luigart R, Pfeifer M, Arzt M. Acute haemodynamic effects of continuous positive airway pressure in awake patients with heart failure.
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