EDITORIAL COMMENT
Colloid osmotic pressure
An under-recognized factor in the clinical syndrome of heart failure*
Marvin A. Konstam, MD, FACC*,*
* Division of Cardiology, Department of Medicine, Tufts-New England Medical Center and Tufts University School of Medicine, Boston, Massachusetts, USA
* Reprint requests and correspondence: Dr. Marvin A. Konstam, Box 108, Tufts-New England Medical Center, 750 Washington Street, Boston, Massachusetts 02111, USA.
MKonstam{at}Tufts-NEMC.org
The clinical syndrome of left heart failure (HF) is often simplistically characterized as dyspnea related to elevation of pulmonary venous pressure. In fact, left HF may manifest as one or a combination of several syndromes, including acute dyspnea, chronic fatigue, functional incapacity, and systemic fluid overload (associated with secondary right HF). Our understanding of the linkage between hemodynamics and these specific clinical manifestations of HF is incomplete. In this issue of the Journal, Arquès et al. (1) have shed light on the importance of serum albumen and plasma oncotic pressure as factors modulating or exacerbating the clinical response to acute elevation of pulmonary artery wedge pressure (PAWP).
The relationship between resting hemodynamic measurements and symptoms of HF is poor. Measurements at rest are poorly predictive of hemodynamic derangement induced during exercise. In the absence of pulmonary congestion, dyspnea often relates to a shift from aerobic to anaerobic metabolism, which occurs at low stress levels in patients with HF, with a dampened cardiac output response to exercise (2). Such a dampened response may be linked to inadequate recruitment of contractility, heart rate, or preload (3–5).
Likewise, the development of pulmonary congestion correlates only roughly with pulmonary venous pressure (approximated by PAWP). A number of factors influence this relationship (6). Patients with chronic HF often manifest little, if any, pulmonary congestion, despite sustained elevation of PAWP. The rate of accumulation of alveolar fluid, for any given hydrostatic pressure, is influenced by the degree of permeability of the alveolar-capillary membrane. Chronic pressure elevation in the pulmonary venous bed may result in thickening of the pulmonary alveolar capillary membrane, protecting the interstitium and air space from transudation of vascular fluid (7–9). Conversely, factors that increase the permeability of the alveolar-capillary membrane will increase the rate of alveolar fluid accumulation at any given hydrostatic gradient (10). Beyond membrane permeability, the rate of accumulation of alveolar fluid is influenced by the rate of pulmonary lymphatic drainage, which tends to increase in response to increases in hydrostatic pressure (11,12).
Arquès et al. (1) bring to light the importance of plasma oncotic pressure as an additional factor influencing the likelihood and degree of pulmonary congestion at a given pulmonary venous pressure. They observed hypoalbuminemia, with a resulting reduction in colloid osmotic pressure (COP), among patients with acute dyspnea due to HF and a normal left ventricular ejection fraction (LVEF), as compared with: 1) patients with acute dyspnea, HF, and a reduced LVEF; 2) those with dyspnea unrelated to HF; and 3) normal subjects. The PAWP tended to be higher in HF patients with a reduced LVEF, resulting in similar COP-PAWP gradients between HF patients with normal and a reduced LVEF. They conclude that in a sizeable proportion of patients presenting with acute dyspnea due to HF, particularly those with a normal LVEF, hypoalbuminemia represents a significant contributing factor.
Patients with HF and a normal LVEF, better characterized as those with the absence of LV cavity dilation (13), generally are elderly patients with long-standing hypertension and concentric LV hypertrophy (14). They tend to be exquisitely sensitive to dietary sodium and volume. In addition to diminished ventricular and vascular compliance, we can now add hypoalbuminemia as a physiologic contributor to the frequent occurrence of acute pulmonary edema in this population.
Observed differences in serum albumen in patients with normal versus reduced LVEF are unlikely to be due to differences in LV function or ventricular volumes, per se. In most cases, the authors attribute hypoalbuminemia to malnutrition or sepsis. Advanced age is likely to predispose to malnutrition, although the difference in average age between those with normal and reduced LVEF in the present study was small. A more detailed exploration of the factors responsible for hypoalbuminemia in this population is warranted.
These findings highlight the differences between community-based populations with HF and those patients enrolled in clinical trials (15). In contrast to patients who have participated in HF trials over the last two decades, the population studied by Arquès et al. (1) was older, with a greater prevalence of comorbidities, including malnutrition and sepsis. These factors are likely to contribute to morbid events for patients in the "real world" far more than within clinical trial populations, in which comorbidities represent criteria for exclusion.
The management of patients with HF requires careful attention to modifiable extra-cardiac contributing factors, including physical conditioning, sodium intake, medication compliance, and social support. Adequate nutrition is known to be important in patients with advanced HF, in whom anorexia and circulating inflammatory cytokines contribute to muscle wasting and increased disability. The findings of Arquès et al. (1) emphasize the complexity of the linkage between cardiac dysfunction and the clinical manifestations of HF. In addition, they further emphasize the importance of maintaining adequate nutrition as we strive to improve clinical outcomes in our patients with HF.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References
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