The heart and lungs are intimately related. Not only do they share the same blood flow and autonomic innervation, they are housed in a common intrathoracic compartment. The heart becomes the passive recipient of the obligatory changes in intrathoracic pressure (ITP) needed to generate tidal breathing and the resultant changes in both venous return to the heart and left ventricular (LV) ejection pressure. ITP decreases with spontaneous inspiratory efforts, causing all cardiac pressures relative to atmosphere to also decrease. Since right atrial pressure is the backpressure to systemic venous return, decreasing right atrial pressure will augment the rate of venous flow by increasing the pressure gradient for venous return. The sudden increase in right ventricular (RV) filling dilates the right ventricle, increases RV output, and often causes the intraventricular septum to shift into the LV cavity, decreasing LV diastolic compliance. If nothing else happens, then LV filling is usually impeded and LV stroke volume and arterial pulse pressure transiently decrease. This inspiration-associated decrease in arterial pulse pressure is commonly referred to as pulsus paradoxus. In patients with obstructive lung disease, the degree of pulsus paradoxus is proportional to the degree of airways obstruction and inspiratory effort.1– With sustained decreases in ITP, however, as may occur with inspiration against an occluded airway (Mueller maneuver), this transient increase in venous return abates as the increased blood flow reaches the left ventricle and the intraventricular septum returns to its neutral position.2 However, the decreasing ITP also increases LV afterload. Since the heart is in the chest, a pressure chamber inside a pressure chamber, changes in ITP will affect the pressure gradient for LV ejection independently of the heart itself. LV ejection occurs into an arterial circuit in which the surrounding pressure is atmospheric pressure, not ITP. A heart in a chest with an ITP of − 20 mm Hg and systolic arterial pressure of 100 mm Hg, for example, is in a pressure well and must generate a full 120 mm Hg to sustain this arterial pressure. Thus, decreases in ITP increase LV afterload. These findings have been known and were well described by Buda et al2– in 1979. This afterload increasing effect of spontaneous inspiratory efforts has been used to explain the development of acute pulmonary edema in patients with severe laryngeal spasm and status asthmaticus. In fact, a dramatic demonstration of the rapidity to which spontaneous inspiration-induced acute LV failure can occur was given by Lemaire et al.3 They showed that acute pulmonary edema rapidly developed in some patients with chronic obstructive lung disease during unsuccessful mechanical ventilation weaning trials. These and other data form the basis for the recommendation that mechanical ventilatory support be continued in patients with cardiovascular insufficiency until their cardiovascular status is stabilized.