Mechanical ventilation is a vital life support treatment for critically ill patients in the intensive care unit, but prolonged use can lead to various adverse events. Therefore, early weaning from the ventilator is essential. However, many weaning attempts fail, increasing morbidity and mortality. Some patients ventilated without cardiac dysfunction may exhibit respiratory symptoms like pulmonary edema during spontaneous breathing trials. This condition, known as weaning-induced pulmonary edema (WiPO), often arises from increased pulmonary artery occlusion pressure due to cardiac insufficiency. During spontaneous breathing, inspiratory efforts in at-risk patients can further diminish pleural pressure, increasing left ventricular afterload and potentially leading to heart failure. Patients with prior heart disease, COPD, the elderly, and the obese are at higher risk for developing WiPO. Early identification of risk factors and cardiac output impairment using bedside echocardiography and pulmonary ultrasound is crucial to promote negative fluid balance, particularly with diuretics. Mechanical ventilation should utilize low tidal volumes to avoid increases in intrathoracic pressure and exacerbation of respiratory effort. To better identify WiPO, high-risk patients should undergo the T-tube spontaneous breathing trial.

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Weaning-Induced Cardiac Failure

  • Saint-Clair Bernardes Neto

摘要

Mechanical ventilation is a vital life support treatment for critically ill patients in the intensive care unit, but prolonged use can lead to various adverse events. Therefore, early weaning from the ventilator is essential. However, many weaning attempts fail, increasing morbidity and mortality. Some patients ventilated without cardiac dysfunction may exhibit respiratory symptoms like pulmonary edema during spontaneous breathing trials. This condition, known as weaning-induced pulmonary edema (WiPO), often arises from increased pulmonary artery occlusion pressure due to cardiac insufficiency. During spontaneous breathing, inspiratory efforts in at-risk patients can further diminish pleural pressure, increasing left ventricular afterload and potentially leading to heart failure. Patients with prior heart disease, COPD, the elderly, and the obese are at higher risk for developing WiPO. Early identification of risk factors and cardiac output impairment using bedside echocardiography and pulmonary ultrasound is crucial to promote negative fluid balance, particularly with diuretics. Mechanical ventilation should utilize low tidal volumes to avoid increases in intrathoracic pressure and exacerbation of respiratory effort. To better identify WiPO, high-risk patients should undergo the T-tube spontaneous breathing trial.