The presence of congestive heart failure can complicate the management of patients who undergo mechanical ventilation. Mechanical ventilation by itself affects the pathophysiology of congestive heart failure by decreasing both the venous return to the heart and cardiac afterload, both of which are well described. In addition, there are other ventilator cardiopulmonary interactions that are less well studied, but may also palliate the severity of heart failure. Withdrawal of mechanical ventilation during weaning reverses the beneficial effects on congestive heart failure of the ventilator. In patients with a low cardiac reserve, it can precipitate myocardial ischemia and worsen heart failure. Patients with poor left ventricular reserve may thus fail weaning attempts despite adequate lung mechanics. Aggressive treatment tailored to the severity of congestive heart failure can facilitate weaning from mechanical ventilation. Monitoring during weaning should be focused on clinical, biochemical, and imaging data that collectively represent the earliest indicators of decompensating heart failure. Treatment strategies include protocol driven weaning and increasing use of noninvasive positive pressure breathing after extubation.
Patients undergoing an exacerbation of congestive heart failure (CHF) can become dependent on mechanical ventilation due to respiratory failure. Weaning from mechanical ventilation under these circumstances becomes feasible with a better understanding of the abnormal gas exchange in CHF and the influence of mechanical ventilation on gas exchange, venous return, and afterload of the heart. The ventilator aids myocardial function in a variety of ways and facilitates gas exchange. Optimization of CHF decreases the dependence of the subject on the ventilator for these salutary effects and facilitates a faster and safer withdrawal of the patient from mechanical ventilation.
From the Department of Medicine, The Texas Lung Injury Institute, The University of Texas Health Science Center, Tyler, TX.
Supported by SI [PO1 HL076406] and The Texas Lung Injury Institute of The University of Texas Health Science Center at Tyler, Tyler, TX.
The authors have nothing to disclose.
Address correspondence to: Joseph J. Padinjarayveetil, MD, The University of Texas Health Science Center at Tyler, 11937 US Hwy 271, Tyler, TX 75708. E-mail: email@example.com.