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Dr. Pinsky is Professor of Anesthesiology and Critical Care, Director of Research, Division of Critical Care Medicine, University of Pittsburgh Medical Center.
Correspondence to: Michael R. Pinsky, MD, FCCP, 606 Scaife Hall, 3550 Terrace St, Pittsburgh, PA 15261; e-mail: pinskymr{at}anes.upmc.edu
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.
Another common group of patients who also experience repetitive profound negative swings in ITP are those with obstructive sleep apnea. Periodic negative swings in ITP of - 20 to - 40 mm Hg two to eight times per minute during these episodes throughout the night are commonplace. Chronic heart failure also develops in these patients. However, the link between obstructive sleep apnea and heart failure is not clear. Several things occur simultaneously during episodes of obstructive sleep apnea. First, not only does ITP decrease, but arterial oxygen saturation declines as well. The combination of arterial desaturation coupled with increased LV afterload may cause long chronic LV dysfunction, although the link between this cause and effect has not been made. Recurrent arterial desaturation also increased pulmonary vascular resistance by the mechanism of hypoxic pulmonary vasoconstriction. If persistent, cor pulmonale also developed. Cor pulmonale is common in patients with severe obstructive sleep apnea (OSA). Importantly, earlier studies by Tkacova et al4 have clearly shown that patients with OSA treated with nighttime continuous positive airway pressure (CPAP) for months display improvement in cardiovascular performance and reduced symptoms of heart failure. Nocturnal CPAP reduces the incidence of both negative swings in ITP and arterial desaturation. Presumably, since the actual increase in ITP induced by CPAP is negligible, most of the benefit of CPAP therapy is due to the prevention of both the large negative swings in ITP and the associated arterial desaturation. However, acute nighttime CPAP sleep studies and long-term nighttime CPAP trials do not allow us to understand which of the processes present is causing the improvement in LV performance. Thus, the relative contribution of the CPAP-induced increases in ITP and arterial saturation on the observed beneficial cardiovascular effects of nocturnal CPAP are not known. In that regard, the study by Bradley et al,5 in the June 2001 issue of CHEST, takes a major step forward in explaining the isolated effect of ITP in cardiac performance.
These workers compared the effect of a Mueller maneuver of - 30 cm H2O on LV performance in nine patients with congestive heart failure (CHF) and nine healthy control subjects. They found that although LV ejection pressure increased equally in both groups, this was followed immediately by a fall in developed pressure in the CHF patients that persisted after release from the strain. Thus, in the absence of hypoxemia, patients with CHF have a prolonged depression in LV performance following a Mueller maneuver as compared to patients without heart failure. Therefore, changes in ITP alone can result in sustained LV depression and may be responsible for the worsening of LV performance over time. Unfortunately, the reasons for the observed sustained LV depression were not studied.
By what mechanisms could transient decreases in ITP induce a persistent depression in LV systolic function? Well, patients with CHF have increased circulating blood volume. Thus, negative swings in ITP will induce a greater increase in venous return than in healthy volunteers. Acute RV dilation would reduce LV end-diastolic volume and, if sustained, make LV stroke volume and developed pressure remain depressed by the Frank-Starling mechanism. Since LV systolic function would be unaltered by this preload-reducing effect, measures of LV performance using the LV end-systolic pressure-volume relation would show no change in the slope of this line, a marker of LV contractility, but a shift of the left ventricle to smaller end-diastolic and end-systolic volumes. This hypothesis can be easily answered by performing an echocardiographic study during the Mueller maneuver to assess intraventricular septal shift and end-diastolic area changes. If LV end-diastolic area, a surrogate for end-diastolic volume, were to decrease, then it would suggest that RV dilation was the primary cause of depressed LV performance. This is an important finding because it would suggest that measures aimed at reducing circulating blood volume would limit LV depression during obstructive sleep apnea episodes by limiting venous return.
Can a Mueller maneuver increase LV afterload, despite a decreasing transmural LV ejection pressure? The answer is yes, depending on what happens simultaneously to LV end-diastolic volume. LV afterload is a difficult concept to define, but in a simple construct, it reflects the maximal wall stress on the LV during ejection. Recall that by the LaPlace theorem, LV wall stress is a function of the product of the transmural pressure and the radius of curvature of the left ventricle. A lower ejection pressure is needed to sustain the same wall stress or afterload as the left ventricle dilates. With increasing wall stress, subendocardial ischemia may develop and will impair LV systolic performance for a while even after the strain phase of the Mueller maneuver is over. Thus, this mechanism also explains the observed data. However, the effect of the Mueller maneuver on LV volumes would be the opposite of the RV dilation hypothesis. Furthermore, some evidence of subendocardial ischemia may be measurable on surface ECGs. Importantly, if this mechanism were the cause of sustained LV depression during OSA episodes, then diuresis alone would be ineffective, and measures aimed at reducing LV afterload, such as pharmacologic reductions in arterial tone and measures aimed at maintaining coronary blood flow, would be the appropriate first lines of treatment outside of preventing the obstructive breaths in the first place.
What have we learned? Not only is spontaneous breathing a form of exercise, requiring increased oxygen delivery to the body, but the negative swings in ITP extract a pressure toll on LV performance. Although of minimal effect transiently in a healthy subject, in patients with preexistent heart failure, the detrimental effects of these negative swings can be sustained long after the obstruction is removed. Considering the frequency of patients with diagnoses of obstructive sleep apnea and the number of patients who complain that their bed partners snore, this may be a greater health hazard than presently considered. In fact, in patients with OAS, it may be that the heart is sleeping with the enemy.
References
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