Why does pulmonary venous pressure rise after onset of LV dysfunction: a theoretical analysis

Abstract

One of the most important consequences of acute left ventricular dysfunction (LVD) is pulmonary edema resulting from a rise in pulmonary venous pressure (PVP). It is generally believed that the PVP rise is a direct hemodynamic consequence of LVD. While this paradigm seems plausible, especially if the LV is viewed as a sump pump, there is no specific evidence to support this simple explanation. A theoretical analysis was performed to assess the hemodynamic mechanisms responsible for the dramatic rise in PVP after acute LVD. The ventricles were modeled as time-varying elastances; pulmonary and systemic vascular systems were modeled as series of resistive and capacitive elements. In response to a 50% decrease in LV contractile strength [end-systolic elastance (Ees)], cardiac output (CO) and mean arterial pressure (MAP) dropped substantially, while PVP increased minimally from its baseline of 12 to approximately 15 mmHg. With LV Ees set at 50% of normal, the effects of sympathetic activation were tested. When heart rate and total peripheral resistance were increased, CO and MAP improved, yet PVP still did not rise. The only intervention that caused a substantial increase in PVP was to simulate the decrease in unstressed volume (VU) of the venous system known to occur with sympathetic activation. When VU was decreased by about 15-20% (comparable to experimentally observed shifts with acute heart failure), PVP increased above 25 mmHg. The effects of pericardial constraints were investigated, and the results suggest a major role of this organ in determining the overall hemodynamic response to acute LVD, sympathetic activation, and explaining the responses to therapy. Thus this analysis suggests that elevations of PVP do not occur simply as a direct hemodynamic consequence of acute LVD. Rather, changes in PVP may be dictated more by sympathetic control on venous capacity. If confirmed, recognition of this as a primary mechanism may prove important in directing development of new therapies and in understanding the mechanisms of disease progression in heart failure.

Development of Heart Failure in Chronic Hypertensive Dahl Rats

“…Although the observations in this study appears to be contrary to traditional teachings about heart failure, they are consistent with more recently proposed concepts of why pulmonary venous pressure increases. 29 Detailed analysis supported by results of animal studies suggests that heart failure can occur as a result of fluid accumulation even if heart function is normal. This is of particular relevance to the current findings obtained in an animal model in which the primary dysfunction is Figure 6.…”

Multiscale model of the human cardiovascular system: Description of heart failure and comparison of contractility indices

“…The fluid mechanics equations that govern such a system are described elsewhere [2,5,6] and only the cardiac pump model will be described in detail in the next section. …”

“…The heart contraction is often described with ad hoc models, like the time-varying elastance model [1,2,3]. Such macroscopic models are not based on the cardiac tissue Email address: sarah.kosta@ulg.ac.be (S. Kosta,) properties and cannot reproduce behaviors that arise from the microscopic scale.…”

A minimal cardiovascular system haemodynamic model for rapid diagnostic assistance

“…Longterm stability was also verified over a period of 40 seconds, or about 66 heartbeats. The patient parameters used in this model are based on those found in the literature, and manipulated to produce model outputs comparable to an average human (Burkhoff, 1993;Chung, 1997). Figure 7 shows the output pressures and volumes for this model while Figure 8 plots the deflection of the septum wall as a result of ventricular interaction.…”