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Abstract

607 ALI = acute lung injury; ARDS = acute respiratory distress syndrome; ARDSexp = extrapulmonary ARDS; ARDSp = pulmonary ARDS; C CW = chest wall compliance; CHF = congestive heart failure; C L = lung compliance; COPD = chronic obstructive pulmonary disease; CPAP = continuous positive airway pressure; ESPVR = end-systolic pressure-volume relationship; FRC = functional residual capacity; IAP = intra-abdominal pressure; ITP = intrathoracic pressure; LV = left ventricular; PaCO2 = arterial carbon dioxide partial pressure; Palv = avleolar pressure; Paw = airway pressure; P CRIT = critical closing pressure; PEEP = positive end-expiratory pressure; Pes = esophageal pressure; Pms = mean systemic pressure; Ppc = pericardial pressure; Ppl = pleural pressure; PVR = pulmonary vascular resistance; RAP = right atrial pressure; RV = right ventricular; SV = stroke volume.Available online http://ccforum.com/content/9/6/607 AbstractIn patients with acute lung injury, high levels of positive endexpiratory pressure (PEEP) may be necessary to maintain or restore oxygenation, despite the fact that 'aggressive' mechanical ventilation can markedly affect cardiac function in a complex and often unpredictable fashion. As heart rate usually does not change with PEEP, the entire fall in cardiac output is a consequence of a reduction in left ventricular stroke volume (SV). PEEP-induced changes in cardiac output are analyzed, therefore, in terms of changes in SV and its determinants (preload, afterload, contractility and ventricular compliance). Mechanical ventilation with PEEP, like any other active or passive ventilatory maneuver, primarily affects cardiac function by changing lung volume and intrathoracic pressure. In order to describe the direct cardiocirculatory consequences of respiratory failure necessitating mechanical ventilation and PEEP, this review will focus on the effects of changes in lung volume, factors controlling venous return, the diastolic interactions between the ventricles and the effects of intrathoracic pressure on cardiac function, specifically left ventricular function. Finally, the hemodynamic consequences of PEEP in patients with heart failure, chronic obstructive pulmonary disease and acute respiratory distress syndrome are discussed.

Influence of Positive End-Expiratory Pressure on Myocardial Strain Assessed by Speckle Tracking Echocardiography in Mechanically Ventilated Patients

“…The main hemodynamic effect of PEEP is the impairment of cardiac function related to lung volume and intrathoracic pressure (ITP) changes [30]. Briefly, when looking at the right side of the heart, the PEEP determines a reduction of the venous return due to an increase in right atrial pressure secondary to increased ITP [30, 31].…”

Associations between positive end-expiratory pressure and outcome of patients without ARDS at onset of ventilation: a systematic review and meta-analysis of randomized controlled trials

“…PEEP affects the loading conditions of the heart [13], as every increase in intrathoracic pressure reduces the preload of the heart and might increase as well as decrease the afterload of the right ventricle depending on whether lung tissue is recruited [13]. The effects of PEEP on cardiac performance could also differ between patients with ARDS and patients without ARDS, as PEEP could reduce right ventricle afterload by preventing or minimizing atelectasis in ARDS patients, while only raising intrathoracic pressure in patients without ARDS [13].…”

“…PEEP affects the loading conditions of the heart [13], as every increase in intrathoracic pressure reduces the preload of the heart and might increase as well as decrease the afterload of the right ventricle depending on whether lung tissue is recruited [13]. The effects of PEEP on cardiac performance could also differ between patients with ARDS and patients without ARDS, as PEEP could reduce right ventricle afterload by preventing or minimizing atelectasis in ARDS patients, while only raising intrathoracic pressure in patients without ARDS [13]. Furthermore, the effects of PEEP on the systemic circulation depend not only on how much lung tissue is recruited but also on lung volume, since if the lung volume is below the functional residual capacity at end expiration, an increase in the level of PEEP likely increases the cardiac output [14].…”

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association

“…Higher pressures, however, may compromise RV preload and increase RV afterload in part through intra-alveolar vessel compression. 234 There are no studies to support one mode of invasive MV over another, and the ideal positive end-expiratory pressure level in patients with CS may depend on the complex cardiopulmonary interplay between RV and LV function, vascular resistance, and fluid status, along with the presence and cause of hypoxemia. Lastly, the ideal oxygenation targets remain undefined, but emerging evidence highlights the potential deleterious effect of hyperoxia in patients with ACS, HF, and OHCA and in general ICU patients.…”