PHILIPPE VIGNON

Overview

Weaning failure is a major complication of mechanical ventilation with associated morbidity and mortality. It is usually defined as an unsuccessful spontaneous breathing trial (SBT) or need for tracheal reintubation within 48 hours following extubation.¹ According to study populations and diagnostic criteria, the incidence of weaning failure ranges from 25% to 42% in large cohorts.¹ Although the mechanisms are varied and potentially complex, failure to wean a critically ill patient from the ventilator frequently has a cardiac origin. Indeed, the transition from positive-pressure ventilation to spontaneous breathing abruptly alters cardiac loading conditions and has been compared with an exercise test that increases cardiac and breathing workload and metabolic expenditure.² Accordingly, patients at high risk for weaning failure have long been identified as those with cardiovascular disease or chronic obstructive pulmonary disease (COPD).^3,4

Echocardiography has progressively supplanted the use of blind, invasive hemodynamic techniques for bedside assessment of central hemodynamics in the intensive care unit (ICU). Because of the real-time, anatomic, and functional information provided on the heart and great vessels, echocardiography is ideally suited for screening the targeted population, assessing the hemodynamic changes induced by SBTs, diagnosing weaning-related pulmonary edema, and identifying its origin. This chapter discusses the clinical value of using echocardiography to assess patients in the ICU at high risk for weaning failure.

Echocardiographic examination

Since transthoracic echocardiography (TTE) is usually informative in this specific clinical setting, transesophageal echocardiography (TEE) is rarely required and performed only as an adjunct to TTE in a patient reconnected to the ventilator. The apical four-chamber view is mainly used to obtain the requested information because it allows evaluation of global and regional ventricular systolic function, left ventricular (LV) diastolic properties and filling pressure, valvular function, intraventricular pressure gradient, and systolic pulmonary artery pressure (Figure 34-1).

Interestingly, TTE may be combined with chest ultrasound to best guide the diagnostic workup of patients with weaning failure at the bedside. After completion of TTE, chest ultrasonography can be performed to obtain valuable morphologic information on the lungs and pleurae, both of which are potentially involved in the weaning failure. For example, chest ultrasonography allows a quantitative diagnosis of pleural effusion and helps in deciding whether to perform thoracentesis in hypoxemic ICU patients.⁵

Hemodynamic changes induced by spontaneous breathing trials

The transition from positive-pressure ventilation to spontaneous breathing abruptly increases ventricular preload and LV afterload, decreases effective LV compliance,³ and may even induce cardiac ischemia.⁶ All these factors tend to increase LV filling pressure, which may result in weaning-induced cardiogenic pulmonary edema, especially in patients with left-sided heart disease.⁷ Nevertheless, in the absence of left heart failure (e.g., COPD patients), the rise in pulmonary artery occlusion pressure (PAOP) remains limited.⁸

In 117 ICU patients fulfilling the criteria for weaning, we performed TTE immediately before and at the end of a 30-minute SBT. The SBT significantly increased LV stroke volume (and hence cardiac output) and LV filling pressure over baseline values as reflected by a higher mitral Doppler E/A ratio and shortened E-wave deceleration time.⁹ Similarly, Ait-Ouffela et al¹⁰ showed that SBTs increase the mitral E/A ratio and shorten the E-wave deceleration time.

Identification of patients at high risk for pulmonary edema during weaning

Echocardiography allows screening of ventilated ICU patients to identify those at high risk for pulmonary edema during weaning. A dilated or hypertrophic cardiomyopathy associated with LV diastolic dysfunction and a relevant left-sided valvulopathy are potential risk factors for weaning-induced pulmonary edema since baseline filling pressure is typically high in these patients and may further increase at the interruption of positive-pressure ventilation.

We previously showed that ICU patients who failed ventilator weaning had a significantly lower LV ejection fraction (median [25th to 75th percentiles]: 36% [27% to 55%] vs. 51% [43% to 55%], P = .04) and higher LV filling pressure (E/E′ ratio: 7.0 [5.0 to 9.2] vs. 5.6 [5.2 to 6.3]; P = .04) before the SBT than did patients who were successfully extubated.⁹ Papanikolaou et al¹¹ reported that a lateral E/E′ ratio higher than 7.8 at baseline (pressure-support ventilation) predicted SBT failure in 50 ventilated ICU patients with a sensitivity and specificity of 79% and 100%, respectively.

Identification of pulmonary edema during weaning

Cardiogenic pulmonary edema induced by weaning from the ventilator is suspected in high-risk patients when alternative causes of weaning failure have been confidently ruled out.⁷ It is a leading cause of weaning failure. In a TTE study performed in 117 ventilated ICU patients, we showed that weaning failure was of cardiac origin in 20 of 23 patients (87%) with an unsuccessful SBT or extubation.⁹ In patients in whom weaning-induced pulmonary edema develops, echocardiography depicts the presence of increased LV filling pressure and helps identify the potential underlying cause to guide therapy.