विवरण
Mechanical ventilation plays a critical role in managing heart failure, especially in acute decompensated cases. It helps reduce the work of breathing, ensuring adequate oxygenation and ventilation when the heart is unable to pump effectively. By decreasing the preload and afterload on the heart, mechanical ventilation aids in improving cardiac output and stabilizing hemodynamics. Additionally, it can alleviate symptoms of respiratory distress and pulmonary edema, providing essential support during the recovery phase. Proper management and timely initiation of mechanical ventilation can significantly enhance patient outcomes in heart failure.
सारांश
- Respiratory failure is common in patients with acute cardiogenic pulmonary edema or cardiogenic shock, resulting from increased pulmonary capillary hydrostatic pressure and fluid filtration exceeding lymphatic drainage capacity, which impairs gas exchange.
- Mechanical ventilation is a lifesaving intervention that can reduce ventricular preload and afterload, decrease extravascular lung water, and lower the work of breathing in patients with decompensated heart failure.
- Initial ventilator settings should include a PEEP of 5 cm water, titrated based on oxygenation, work of breathing, and hemodynamics. Tidal volume is typically set at 6-8 ml/kg, but can be lower in certain conditions like ARDS. FiO2 starts high and is reduced promptly to avoid adverse effects.
- Positive pressure ventilation reduces venous return and preload to both ventricles, decreases left ventricular afterload, but can increase right ventricular afterload due to mechanical compression of pulmonary vessels. It also reduces the work of breathing.
- PEEP helps keep alveoli open, improving oxygenation and decreasing extravascular lung water. Incremental increases of PEEP are guided by hemodynamic monitoring and indicators of end-organ perfusion.
- Inspiratory support with mechanical ventilation offloads the work of breathing in non-compliant lungs, allowing limited cardiac output to better meet non-pulmonary metabolic needs.
- Maintaining plateau pressure below 30 cm water minimizes barotrauma risk, such as pneumothorax and pneumomediastinum. High peak inspiratory pressure indicates resistance, such as bronchospasm or tube obstruction.
- Excessive supplemental oxygen can lead to oxygen free radical formation, worsening cardiac abnormalities, and causing intracellular calcium overload and cardiac hypertrophy. The FiO2 should ideally be less than 50% to avoid free radical damage, and the target oxygen saturation should be 92-96%.
- Modes like volume assured pressure support (VAPS), proportional assist ventilation (PAV), and neurally adjusted ventilatory assist (NAVA) can improve patient-ventilator synchrony. Newer modes like adaptive support ventilation (ASV) adjust pressure support to maintain minute ventilation and SmartCare ventilation automatically wean the patient.
- Winning from ventilation should be done during daytime, and switching to non-invasive ventilation after extubation may shorten ICU stay and lower mortality. Gradual pressure support reduction or daily T-piece trials can assess tolerance. Heart failure and fluid balance are predictors of extubation failure.
- Optimizing pre- and post-extubation care includes prophylactic non-invasive positive pressure ventilation (NIV) for at least eight hours per day for the first 48 hours, continuous breathing trials, and optimizing preload, afterload, and inotropic support to prevent reintubation.
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